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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Anandalakshmi, Venkatraman, Guillaume Hochart, David Bonnel, Jonathan Stauber, Shigeto Shimmura, Rajamani Lakshminarayanan, Konstantin Pervushin, and Jodhbir S. Mehta. "Targeted Expression of TGFBIp Peptides in Mouse and Human Tissue by MALDI-Mass Spectrometry Imaging." Separations 8, no. 7 (July 3, 2021): 97. http://dx.doi.org/10.3390/separations8070097.

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Stromal corneal dystrophies are a group of hereditary disorders caused by mutations in the TGFBI gene. The mutant TGFBIp is prone to protein aggregation and the mutant protein gets deposited in the cornea, leading to severe visual impairment. The mutations lead to a corneal specific protein aggregation suggesting the involvement of tissue-specific factors. The exact molecular mechanism of the process of tissue-specific protein aggregation remains to be elucidated. Differential proteolysis of mutant TGFBIp is a critical component of the disease pathology. The differential proteolysis gives rise to shorter peptides that are highly aggregation-prone and initiate the aggregation cascade. Analyzing the proteolytic processing of the different TGFBIp mutant may provide insight to aid in understanding the amyloid aggregation mechanism. We developed a MALDI-MSI methodology to identify expression and spatial localization of TGFBIp peptides in the cornea. Corneal tissue samples were collected from both control and dystrophic patients (with 2 different mutations), embedded in OCT and sectioned. The sections were trypsin digested and subjected to mass spectrometry imaging using a targeted approach to detect TGFBIp. MALDI-MSI identified peptides from TGFBIp that co-localized with the amyloid corneal deposits. In addition to the relative abundance data, the specific location of the peptides across the corneal sections as molecular signatures was also identified. Spatial distribution and intensity of the TGFBIp peptides showed differences between diseased and control models but also between the two LCD phenotypes. The TGFBIp peptide with m/z of 787.474 and m/z of 1179.579 showed increased expression in both LCD mutants compared to the controls. The peptide with m/z of 929.5 showed increased expression in the LCD phenotype with H626R mutation while the peptide with m/z of 1315.802 was abundant in the sample with R124C mutation. This initial report of 2D spatial protein signature and localization of TGFBIp may be expanded to other mutations to understand the proteolytic patterns of TGFBIp in different mutations.
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2

Miyakawa, Ayumi A., Thais Girão-Silva, Jose E. Krieger, and Elazer R. Edelman. "Rapamycin activates TGF receptor independently of its ligand: implications for endothelial dysfunction." Clinical Science 132, no. 4 (February 16, 2018): 437–47. http://dx.doi.org/10.1042/cs20171457.

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Rapamycin, the macrolide immunosuppressant and active pharmaceutic in drug-eluting stents (DES), has a well-recognized antiproliferative action that involves inhibition of the mTOR pathway after binding to the cytosolic protein FKBP12. TGF receptor-type I (TGFRI) spontaneous activation is inhibited by the association with FKBP12. We hypothesized that rapamycin, in addition to inhibition of mTOR signaling, activates TGFRI independent of TGFβ. Human umbilical vein endothelial cells (HUVECs) were treated with rapamycin (10 nmol/l) and/or TGFβ RI kinase inhibitor (TGFRIi, 100 nmol/l) for 24 h. Rapamycin induced SMAD phosphorylation (SMAD1, SMAD2, and SMAD5) and PAI-1 up-regulation, which was specifically abrogated by SMAD2 knockdown. TGFRIi efficiently blocked phosphorylation of SMAD2, but not SMAD1/5. Interestingly, the inhibitor did not alter cell proliferation arrest induced by rapamycin. Active TGFβ secretion was not affected by the treatment. Neutralizing TGFβ experiments did not influence SMAD2 phosphorylation or PAI-1 expression indicating that activation of this pathway is independent of the ligand. In addition, rapamycin induction of endothelial-to-mesenchymal transition (EndMT) was potentiated by IL-1β and efficiently blocked by TGFRIi. In vivo, the prothrombogenic effects of rapamycin and up-regulation of PAI-1 in murine carotid arteries were reduced by TGFRIi treatment. In conclusion, we provide evidence that rapamycin activates TGF receptor independent of its ligand TGFβ, in concert with promotion of PAI-1 expression and changes in endothelial phenotype. These undesirable effects, the prothrombogenic state, and activation of EndMT are SMAD2-dependent and independent of the therapeutic rapamycin-induced cell proliferation arrest.
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3

Pereira, Marcelo de Souza Fernandes, Yasemin Sezgin, Aarohi Thakkar, and Dean Anthony Lee. "Tgfβ-Imprinting Decrease CD38 Expression and Lead to Metabolic Reprogramming on Primary NK Cell." Blood 136, Supplement 1 (November 5, 2020): 4. http://dx.doi.org/10.1182/blood-2020-143085.

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Transforming growth factor-β (TGF-β) plays an essential role in regulating immune responses through its immunossupressive effect on adaptive and innate immune cells. In addition, we and others have shown that alterations in cell-intrinsic metabolism profiles can significantly impact the function of immune cells. Previously, our group demonstrated that TGFβ-imprinting (TGFβi) decreases NK cell sensitivity to TGFβ through SMAD3 suppression and enhances a pro-inflammatory phenotype with hypersecretion of IFN-γ, TNF-α, and GM-CSF, which appeared to be mediated by an epigenetic mechanism. To evaluate this process, we conducted RNA-seq and ATAC-seq to evaluate the impact of chromosomal remodeling on gene expression. In addition to confirming low SMAD3 transcription, this data showed that TGFβi NK cells have decreased CD38 expression, which we confirmed at the protein level. Since CD38 is an ectoenzyme that regulates nicotinamide adenine dinucleotide (NAD+), a critical component of OXPHOS in both T and NK cells, we examined the effect of TGFβi on NK cell metabolism. TGFβi primary NK cells were generated from peripheral blood of healthy donors as previously described, and using a mitochondrial stress test assay, we observed higher oxygen consumption rates (OCR). However, in the glycolysis stress test assay we observed comparable extracellular acidification rates (ECAR) between Standard expanded and TGFbi NK cells, resulting in higher OCR/ECAR ratios in TGFbi NK cells. Since TGFβ has been shown to induce fragmented mitochondria, and inhibition of mitochondrial fragmentation improved mitochondrial metabolism, we evaluated subcellular structure of TGFβi NK cellsby transmission electron microscopy (TEM). We found no difference in mitochondrial fragmentation between STD and TGFβi NK cells. Together, these results show that TGFβi induces epigenetic reprograming of NK cells that results in increased OXPHOS through CD38 suppression. Moreover, the decreases CD38 expression in TGFβi NK cells could be a promising non-genetic alternative to generating CD38-negative NK cells to avoid fratricide in combination with DARA Figure Disclosures Lee: Kiadis Pharma Netherlands B.V: Consultancy, Current equity holder in publicly-traded company, Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.
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4

Lee, In-Chul, and Jong-Sup Bae. "Suppressive Effects of Sulforaphane on TGFBIp-mediated Sepsis." Natural Product Communications 12, no. 10 (October 2017): 1934578X1701201. http://dx.doi.org/10.1177/1934578x1701201026.

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Sulforaphane (SFN) is produced when the enzyme myrosinase transforms glucoraphanin upon damage to the plant such as from chewing and effective in preventing carcinogenesis, diabetes, and inflammatory responses. Transforming growth factor β-induced protein (TGFBIp) is an extracellular matrix protein whose expression in several cell types is greatly increased by TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. We hypothesized that SFN could reduce TGFBIp-mediated severe inflammatory responses in human endothelial cells and mice. Here, we investigated the anti-septic effects and underlying mechanisms of SFN against TGFBIp-mediated septic responses. SFN effectively inhibited lipopolysaccharide-induced release of TGFBIp and suppressed TGFBIp-mediated septic responses. In addition, SFN suppressed cecal ligation and puncture (CLP)-induced sepsis lethality and pulmonary injury. In conclusion, SFN suppressed TGFBIp-mediated and CLP-induced septic responses. Therefore, SFN could be a potential therapeutic agent for treatment of various severe vascular inflammatory diseases via inhibition of the TGFBIp signaling pathway.
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5

Kim, Ha-Jeong, Suyeon Rhe, and Haeuk Jung. "Platelet TGFBIp induces foam cell formation after platelet phagocytosis." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 206.26. http://dx.doi.org/10.4049/jimmunol.198.supp.206.26.

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Abstract Foam cells play a critical role in the atherosclerosis development. It is reported that platelets phagocytosis induces foam cell formation by producing more inflammatory cytokines. However, platelet induced foam cell formation mechanism is not clear. TGFBIp is a secreted extracellular matrix protein that is consisted by 4 fasciclin-1 domains. TGFBIp is produced by several cells include macrophages and works as chemoattractant to monocytes. TGFBIp is also in the platelet granule and it is secreted and bound on platelets when platelets are activated. Platelets are removed by macrophages when they are activated. However, the role of TGFBIp on activated platelets is not clear. In this report, we used TGFBIp lacking platelets to investigate the role of TGFBIp in platelets. When macrophages uptake TGFBIp lacking platelets, foam cell formation is less than WT platelets are uptaken.
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6

Kim, Ha-Jeong, Pan-Kyung Kim, Sang Mun Bae, Hye-Nam Son, Debraj Singh Thoudam, Jung-Eun Kim, Byung-Heon Lee, Rang-Woon Park, and In-San Kim. "Transforming growth factor-β–induced protein (TGFBIp/β ig-h3) activates platelets and promotes thrombogenesis." Blood 114, no. 25 (December 10, 2009): 5206–15. http://dx.doi.org/10.1182/blood-2009-03-212415.

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Abstract Transforming growth factor-β–induced protein (TGFBIp)/βig-h3 is a 68-kDa extracellular matrix protein that is functionally associated with the adhesion, migration, proliferation, and differentiation of various cells. The presence of TGFBIp in platelets led us to study the role of this protein in the regulation of platelet functions. Upon activation, platelet TGFBIp was released and associated with the platelets. TGFBIp mediates not only the adhesion and spread of platelets but also activates them, resulting in phosphatidylserine exposure, α-granule secretion, and increased integrin affinity. The fasciclin 1 domains of TGFBIp are mainly responsible for the activation of platelets. TGFBIp promotes thrombus formation on type I fibrillar collagen under flow conditions in vitro and induces pulmonary embolism in mice. Moreover, transgenic mice, which have approximately a 1.7-fold greater blood TGFBIp concentration, are significantly more susceptible to collagen- and epinephrine-induced pulmonary embolism than wild-type mice. These results suggest that TGFBIp, a human platelet protein, plays important roles in platelet activation and thrombus formation. Our findings will increase our understanding of the novel mechanism of platelet activation, contributing to a better understanding of thrombotic pathways and the development of new antithrombotic therapies.
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7

Jeong, Seongdo, Sae-Kwang Ku, and Jong-Sup Bae. "Anti-inflammatory effects of pelargonidin on TGFBIp-induced responses." Canadian Journal of Physiology and Pharmacology 95, no. 4 (April 2017): 372–81. http://dx.doi.org/10.1139/cjpp-2016-0322.

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Transforming growth factor β induced protein (TGFBIp) is an extracellular matrix protein expressed in several cell types in response to TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. Pelargonidin (PEL) is a well-known red pigment found in plants, and has been reported as having important biological activities that are potentially beneficial for human health. This study was undertaken to investigate whether PEL can modulate TGFBIp-mediated inflammatory responses in HUVECs and in mice. The anti-inflammatory activities of PEL were determined by measuring permeability, leukocyte adhesion and migration, and activation of proinflammatory proteins in TGFBIp-activated HUVECs and mice. In addition, the beneficial effects of PEL on survival rate in a mouse sepsis model were tested. We found that PEL inhibited TGFBIp-induced barrier disruption, expression of cell adhesion molecules and adhesion/transendothelial migration of neutrophils to human endothelial cells. PEL also suppressed TGFBIp-induced hyperpermeability and leukocyte migration in vivo. These results suggest that PEL possesses anti-inflammatory properties that result in inhibition of hyperpermeability, expression of cell adhesion molecules, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.
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8

Park, Hee Ho, Hong Nam Kim, Hyelim Kim, Youngbum Yoo, Hyosoo Shin, Eun Young Choi, Jong-Sup Bae, and Wonhwa Lee. "Acetylated K676 TGFBIp as a severity diagnostic blood biomarker for SARS-CoV-2 pneumonia." Science Advances 6, no. 31 (July 2020): eabc1564. http://dx.doi.org/10.1126/sciadv.abc1564.

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The outbreak of the highly contagious and deadly severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as coronavirus disease 2019 (COVID-19), has posed a serious threat to public health across the globe, calling for the development of effective diagnostic markers and therapeutics. Here, we report a highly reliable severity diagnostic biomarker, acetylated 676th lysine transforming growth factor–beta–induced protein (TGFBIp K676Ac). TGFBIp K676Ac was consistently elevated in the blood of patients with SARS-CoV-2 pneumonia (n = 113), especially in patients in the intensive care unit (ICU) compared to non-ICU patients. Patients’ blood samples showed increased cytokines and lymphopenia, which are exemplary indicators of SARS-CoV-2 pneumonia. Treatment with TGFBIp neutralizing antibodies suppressed the cytokine storm. The increased level of TGFBIp K676Ac in ICU patients suggests the promise of this protein as a reliable severity diagnostic biomarker for severe SARS-CoV-2 disease.
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9

Nam, Sang Min, Yong-Sun Maeng, Eung Kweon Kim, Kyoung Yul Seo, and Helen Lew. "Ex Vivo Expansion of Human Limbal Epithelial Cells Using Human Placenta-Derived and Umbilical Cord-Derived Mesenchymal Stem Cells." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4206187.

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Ex vivo culture of human limbal epithelial cells (LECs) is used to treat limbal stem cell (LSC) deficiency, a vision loss condition, and suitable culture systems using feeder cells or serum without animal elements have been developed. This study evaluated the use of human umbilical cord or placenta mesenchymal stem cells (C-MSCs or P-MSCs, resp.) as feeder cells in an animal/serum-free coculture system with human LECs. C-/P-MSCs stimulated LEC colony formation of the stem cell markers (p63, ABCG2) and secreted known LEC clonal growth factors (keratinocyte growth factor, β-nerve growth factor). Transforming growth factor-β-induced protein (TGFBIp), an extracellular matrix (ECM) protein, was produced by C-/P-MSCs and resulted in an increase in p63+ ABCG2+ LEC colonies. TGFBIp-activated integrin signaling molecules (FAK, Src, and ERK) were expressed in LECs, and TGFBIp-induced LEC proliferation was effectively blocked by a FAK inhibitor. In conclusion, C-/P-MSCs enhanced LEC culture by increasing growth of the LSC population by secreting growth factors and the ECM protein TGFBIp, which is suggested to be a novel factor for promoting the growth of LECs in culture. C-/P-MSCs may be useful for the generation of animal-free culture systems for the treatment of LSC deficiency.
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10

Sørensen, Charlotte S., Kasper Runager, Carsten Scavenius, Morten M. Jensen, Nadia S. Nielsen, Gunna Christiansen, Steen V. Petersen, Henrik Karring, Kristian W. Sanggaard, and Jan J. Enghild. "Fibril Core of Transforming Growth Factor Beta-Induced Protein (TGFBIp) Facilitates Aggregation of Corneal TGFBIp." Biochemistry 54, no. 19 (May 6, 2015): 2943–56. http://dx.doi.org/10.1021/acs.biochem.5b00292.

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11

Kim, Ha-Jeong, Pan-Kyung Kim, Sang-Mun Bae, Hey-Nam Son, Thoudam D. Singh, Jung-Eun Kim, and In-San Kim. "TGFBIp activates platelets and promotes thrombogenesis." Matrix Biology 27 (December 2008): 44–45. http://dx.doi.org/10.1016/j.matbio.2008.09.360.

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12

Rowley, Jesse W., Andrew S. Weyrich, and Robert A. Campbell. "TGFBIp: more than meets the eye?" Blood 114, no. 25 (December 10, 2009): 5113–14. http://dx.doi.org/10.1182/blood-2009-09-243881.

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13

Venkatraman, Anandalakshmi, Minh-Dao Duong-Thi, Konstantin Pervushin, Sten Ohlson, and Jodhbir Singh Mehta. "Pharmaceutical modulation of the proteolytic profile of Transforming Growth Factor Beta induced protein (TGFBIp) offers a new avenue for treatment of TGFBI-corneal dystrophy." Journal of Advanced Research 24 (July 2020): 529–43. http://dx.doi.org/10.1016/j.jare.2020.05.012.

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14

Kim, Ha-Jeong, and In-San Kim. "TGFBIp promotes monocytes adhesion, migration and chemotaxis." Matrix Biology 27 (December 2008): 44. http://dx.doi.org/10.1016/j.matbio.2008.09.358.

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15

Lin, Tong, Xiaozhao Zhang, Yang Lu, and Lan Gong. "TGFBIp mediates lymphatic sprouting in corneal lymphangiogenesis." Journal of Cellular and Molecular Medicine 23, no. 11 (August 28, 2019): 7602–16. http://dx.doi.org/10.1111/jcmm.14633.

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16

Song, Xiaojun, Lu Cai, Yafang Li, Jiu Zhu, Ping Jin, Liming Chen, and Fei Ma. "Identification and characterization of transforming growth factor β induced gene (TGFBIG) from Branchiostoma belcheri: Insights into evolution of TGFBI family." Genomics 103, no. 1 (January 2014): 147–53. http://dx.doi.org/10.1016/j.ygeno.2013.10.002.

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17

SOMARAKICORMIER, M., and R. ZAMILPA. "A model of the biological functions of TGFβIp." Matrix Biology 25 (November 2006): S91. http://dx.doi.org/10.1016/j.matbio.2006.08.249.

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18

Son, Hye-Nam, Ju-Ock Nam, and In-San Kim. "TGFBIp/ βig-h3, an endogenous anti-angiogenic molecule." Matrix Biology 27 (December 2008): 16. http://dx.doi.org/10.1016/j.matbio.2008.09.246.

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19

LeBaron, Richard G., Maria Somaraki-Cormier, Clyde F. Phelix, Rajesha Rupaimoole, Christine L. Miller, and Rogelio Zamilpa. "TGFBIp C-terminal fragment induces osteosarcoma cell apoptosis." Matrix Biology 27 (December 2008): 51–52. http://dx.doi.org/10.1016/j.matbio.2008.09.389.

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20

Somaraki-Cormier, Maria, Rogelio Zamilpa, and Richard G. LeBaron. "TGFBIp interacts with type I collagen in vitro." Matrix Biology 27 (December 2008): 52. http://dx.doi.org/10.1016/j.matbio.2008.09.390.

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21

Choi, Seung-il, Yong-Sun Maeng, Tae-im Kim, Yangsin Lee, Yong-Sun Kim, and Eung Kweon Kim. "Lysosomal Trafficking of TGFBIp via Caveolae-Mediated Endocytosis." PLOS ONE 10, no. 4 (April 8, 2015): e0119561. http://dx.doi.org/10.1371/journal.pone.0119561.

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22

Guo, Shi-Kun, Ming-Feng Shen, Hong-Wei Yao, and Yong-Sheng Liu. "Enhanced Expression of TGFBI Promotes the Proliferation and Migration of Glioma Cells." Cellular Physiology and Biochemistry 49, no. 3 (2018): 1138–50. http://dx.doi.org/10.1159/000493293.

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Background/Aims: Transforming growth factor beta-induced protein (TGFBI) is an extracellular matrix protein induced by TGF-β. Previous studies have reported that the abnormal expression of TGFBI is related to the occurrence and development of some types of cancers, while the role of TGFBI in glioma is uncertain. Methods: The association between TGFBI expression and the prognosis of patients with glioma was analyzed based on data obtained from The Cancer Genome Atlas database. TGFBI expression was analyzed in 3 normal human brains and 57 cases of human gliomas by immunohistochemistry followed by an evaluation of the relationships between TGFBI expression and clinic-pathological features. Furthermore, the RNA interference plasmid pSUPER-shTGFBI was constructed and transfected into U87 and U251 cells to explore the effect of short hairpin RNA against TGFBI (shTGFBI) on cell proliferation, migration, invasion and apoptosis. Western blot analysis was performed to examine the expression of proteins related to apoptosis and proteins in the PI3K/Akt signaling pathway. Results: High TGFBI expression was found to be associated with poor prognosis in patients with glioblastoma multiforme. Immunohistochemistry showed that TGFBI expression was significantly higher in glioma tissue than in normal human brain tissues. The expression level of TGFBI showed no significant correlation with age, sex, lymph-node metastasis, or pathological grade. sh-TGFBI could inhibit proliferation, invasion and migration and induce apoptosis in U87 and U251 cells in vitro. Furthermore, the phosphorylation levels of AKT and mTOR declined significantly in sh-TGFBI transfected U81 and U251 cells when compared with control. Conclusion: TGFBI was up-regulated in glioma cells and played a promoting role in the growth and motility of U87 and U251 cells. These results suggested that TGFBI has the potential to be a diagnostic marker and to serve as a target for the treatment of gliomas.
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23

Bocharov, Alexander, Irina Luzina, Virginia Lockatell, Kendrick Highsmith, and Sergei Atamas. "IL-4 stimulates production of TGF-β-induced (TGFBI) mRNA and protein in T cells but not in monocytes, fibroblasts, or pulmonary epithelial cells (44.16)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 44.16. http://dx.doi.org/10.4049/jimmunol.184.supp.44.16.

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Abstract TGFBI is an extracellular matrix and an adhesion protein produced by a variety of cell types. It is not known whether cytokines other than TGF-β may regulate TGFBI production. RT-Q-PCR and Western blotting assays revealed production of TGFBI mRNA and protein, respectively, in cultured purified primary monocytes, primary pulmonary fibroblasts, and a pulmonary epithelial cell line A549. Stimulation of these cultures with 300 ng/ml of rhIL-4 did not cause a significant change in TGFBI mRNA after 3, 6, 12, or 24 h, or in TGFBI protein after 24 or 48h, (p > 0.05 in all cases, two separate cell donors tested each on two independent occasions). Primary T cell (> 95% purity) cultured from 4 separate donors and tested each on at least three occasions produced basal TGFBI mRNA and protein, although at the levels 10-15 fold below those observed in other tested cell types. Stimulation of T cells or PBMC with IL-4 revealed time dependent increases in the steady-state level of TGFBI mRNA and protein, but not in TGF-β mRNA. The maximal effect of IL-4 on TGFBI mRNA (2-6 fold increase, p < 0.05) was observed at 3 h and 6 h; and on TGFBI protein at 24 and 48 h of stimulation. The effect of IL-4 on TGFBI production was not attenuated by a TGF-β-blocking antibody 1D11. Thus, IL-4 induces TGFBI production in T cells in a TGF-β-independent fashion. T cells may use TGFBI as an adhesion molecule for binding to known TGFBI receptors integrins αVβ3, αVβ5, and α3β1, collagens, and fibronectin.
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24

Yellore, Vivek S., Sylvia A. Rayner, and Anthony J. Aldave. "TGFB1-Induced Extracellular Expression of TGFBIp and Inhibition of TGFBIp Expression by RNA Interference in a Human Corneal Epithelial Cell Line." Investigative Opthalmology & Visual Science 52, no. 2 (February 9, 2011): 757. http://dx.doi.org/10.1167/iovs.10-5362.

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25

Ryu, Soo Ho, Chaeyeong Kim, Nayeon Kim, Wonhwa Lee, and Jong-Sup Bae. "Inhibitory functions of cornuside on TGFBIp-mediated septic responses." Journal of Natural Medicines 76, no. 2 (January 13, 2022): 451–61. http://dx.doi.org/10.1007/s11418-021-01601-2.

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26

Maeng, Y.-S., B. Aguilar, S.-I. Choi, and E. K. Kim. "Inhibition of TGFBIp expression reduces lymphangiogenesis and tumor metastasis." Oncogene 35, no. 2 (March 16, 2015): 196–205. http://dx.doi.org/10.1038/onc.2015.73.

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27

Tai, Tak Yee Tania, Mausam R. Damani, Rosalind Vo, Sylvia A. Rayner, Ben J. Glasgow, John D. Hofbauer, Richard Casey, and Anthony J. Aldave. "Keratoconus Associated With Corneal Stromal Amyloid Deposition Containing TGFBIp." Cornea 28, no. 5 (June 2009): 589–93. http://dx.doi.org/10.1097/ico.0b013e31818c9003.

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Jung, Byeongjin, Sae-Kwang Ku, and Jong-Sup Bae. "Ameliorative effect of methylthiouracil on TGFBIp-induced septic responses." Biochemical and Biophysical Research Communications 463, no. 4 (August 2015): 661–66. http://dx.doi.org/10.1016/j.bbrc.2015.05.120.

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Lee, In-Chul, and Jong-Sup Bae. "Antiseptic effects of dabrafenib on TGFBIp-induced septic responses." Chemico-Biological Interactions 278 (December 2017): 92–100. http://dx.doi.org/10.1016/j.cbi.2017.10.016.

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30

Min, Gahee, Sae-Kwang Ku, Taeho Lee, and Jong-Sup Bae. "Suppressive effects of zingerone on TGFBIp-mediated septic responses." Archives of Pharmacal Research 41, no. 3 (May 16, 2017): 276–87. http://dx.doi.org/10.1007/s12272-017-0919-9.

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31

Yang, Lingmin, Ranliang Cui, Yueguo Li, Kai Liang, Min Ni, and Yajun Gu. "Hypoxia-Induced TGFBI as a Serum Biomarker for Laboratory Diagnosis and Prognosis in Patients with Pancreatic Ductal Adenocarcinoma." Laboratory Medicine 51, no. 4 (October 18, 2019): 352–61. http://dx.doi.org/10.1093/labmed/lmz063.

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Abstract Objective To explore novel biomarkers for patients with pancreatic ductal adenocarcinoma (PDAC), from the perspective of tumor hypoxia. Methods We screened 29 differentially expressed and hypoxia-upregulated genes from the Oncomine database. A total of 12 secretory proteins that interact with hypoxia-inducible factor 1 (HIF-1A) were selected by STRING (protein-protein interaction networks). After excluding enzymes and collagens, insulin-like growth factor-binding protein 3 (IGFBP3), glycoprotein NBM (GPNMB), transforming growth factor–β-induced (TGFBI), and biglycan (BGN) were detected by sandwich enzyme-linked immunosorbent assay (ELISA) in patients with cancer and healthy control individuals. Results The serum level of TGFBI was significantly elevated in patients with PDAC, compared with healthy controls; the assay could discriminate among cases of PDAC in different clinical stages. The amount of TGFBI was significantly decreased after treatment. The combination of TGFBI and cancer antigen (CA) 19-9 was more accurate than TGFBI or CA 19-9 alone as diagnostic markers. Also, TGFBI might be used as a prognostic marker according to the PROGgeneV2 Pan Cancer Prognostics Database. Conclusions Serum TGFBI, combined with CA 19-9, offers higher diagnostic value than other methods for patients with PDAC. Also, TGFBI might be used as a prognostic marker.
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32

Gao, Jianchao, Lexue Fei, Xiaotang Wu, and Hua Li. "MiR-766-3p Suppresses Malignant Behaviors and Stimulates Apoptosis of Colon Cancer Cells via Targeting TGFBI." Canadian Journal of Gastroenterology and Hepatology 2022 (January 17, 2022): 1–8. http://dx.doi.org/10.1155/2022/7234704.

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Background. MicroRNAs (miRNAs) can affect the progression of colon cancer cells. A variety of miRNAs, especially miR-766-3p, are proved to be abnormally expressed in colon cancer, but the molecular mechanism of miR-766-3p in this cancer has not yet been fully defined. Methods. Differentially expressed genes in the TCGA-COAD dataset were searched through bioinformatics analysis. MiR-766-3p and TGFBI mRNA levels were measured by qRT-PCR. TGFBI protein expression was measured via Western blot. Targeting relation between miR-766-3p and TGFBI was investigated by dual-luciferase reporter gene assay. Cell proliferation, invasion migration, and apoptosis were detected by cell functional assays. Results. MiR-766-3p was less expressed, while TGFBI was conspicuously highly expressed in colon cancer. MiR-766-3p high expression suppressed cell malignant behaviors and induced cell apoptosis in colon cancer. MiR-766-3p had a targeting relation with TGFBI verified by dual-luciferase assay. The cancer-suppressive impact of miR-766-3p overexpression was attenuated by overexpressing TGFBI. Conclusions. MiR-766-3p/TGFBI axis suppressed malignant behaviors and facilitated apoptosis of colon cancer cells. MiR-766-3p may be an underlying target for colon cancer.
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Ween, M., P. Hoffmann, R. J. Rodgers, C. Ricciardelli, and M. K. Oehler. "510. TRANSFORMING GROWTH FACTOR INDUCED PROTEIN TGFβI PROMOTES OVARIAN CANCER CELL MOTILITY AND ADHESION TO PERITONEAL CELLS." Reproduction, Fertility and Development 21, no. 9 (2009): 109. http://dx.doi.org/10.1071/srb09abs510.

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Ovarian cancer is characterized by metastases to the peritoneal surface lining the abdominal cavity. It remains unclear which factors promote the implantation of ovarian cancer cells onto the peritoneal lining. We have recently investigated interactions between ovarian cancer cells (OVCAR-5, OVCAR-3, and SKOV-3) and mesothelial cells isolated from omental tissues (LP-9). We conducted a proteomic screen of the conditioned medium of co-cultures of ovarian cancer and mesothelial cells. One of the molecules identified to be modulated is the extracellular matrix adhesion protein, transforming growth factor-beta-induced protein (TGFβI, also known as b ig-H3 or keratoepithelin) which is induced by transforming growth factor-beta in many cell types which has been shown to promote adhesion and migration of hepatoma and astrocytoma cells and enhance colon cancer cell extravasation. In this study we investigated the expression of TGFβI in ovarian cancer tissues and the effects of recombinant TGFβI on ovarian cancer motility and adhesion to peritoneal mesothelial cells. In functional assays, treatment with recombinant TGFβI significantly increased adhesion of all three ovarian cancer cell lines to LP-9 mesothelial cells by up to 25% (P<0.01) and increased motility in OVCAR-5 cells by 62% (P<0.001). Furthermore, addition of a neutralising TGFβI antibody reduced OVCAR-5 adhesion to LP-9 to 79% of control level (P<0.001). TGFβI produced by LP-9 cells was processed to smaller forms when co-cultured with ovarian cancer cell lines by western blotting. MALDI-TOF/TOF mass spectrometry identified TGFβI processing at both the N and C terminal domains. The addition of broad spectrum protease inhibitors blocked the TGFβI processing and reduced OVCAR-5 adhesion to LP-9 cells to 60% of control level (P<0.001). We conclude that although some ovarian cancer cells produce low levels of TGFβI, TGFβI abundantly expressed by peritoneal mesothelial cells can promote ovarian cancer cell adhesion and motility.
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Zhao, Feng, Yuan Liu, and Tao Guan. "Analysis of TGFBI Gene Mutations in Three Chinese Families with Corneal Dystrophy." Journal of Ophthalmology 2019 (January 22, 2019): 1–9. http://dx.doi.org/10.1155/2019/6769013.

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Objective. To identify the types of TGFBI (transforming growth factor, beta-induced) gene mutations in three Chinese families with Reis–Bücklers corneal dystrophy (RBCD), lattice corneal dystrophy type I (LCDI), or Avellino corneal dystrophy (ACD) and to investigate the relationship between the phenotypes and genotypes of corneal dystrophy. Methods. Peripheral blood was collected from 24 patients and 76 phenotypically normal members in three Chinese families as well as from 100 healthy controls. Genomic DNA was extracted. All 17 exons of the TGFBI gene, and the exon-intron junctions were examined by polymerase chain reaction (PCR) and direct DNA sequencing to identify and analyse gene mutations. In addition, all members of the three families were subjected to detailed clinical examinations. Results. The heterozygous c.371G > T (p.R124L) mutation was detected in exon 4 of the TGFBI gene in nine patients from the family with RBCD. In contrast, this mutation was not found in the phenotypically normal members of the family. The heterozygous c.370C > T (p.R124C) mutation was found in exon 4 of the TGFBI gene in 11 patients from the family with LCDI. This mutation was not found in the phenotypically normal members of the family. The heterozygous c.371G > A (p.R124H) mutation was detected in exon 4 of the TGFBI gene in four patients from the family with ACD. Again, this mutation was not found in the phenotypically normal members of the family. The TGFBI gene mutations cosegregated with the disease phenotypes in the three families and exhibited an autosomal dominant mode of inheritance. No TGFBI gene mutations were detected in the 100 healthy controls. Conclusion. There is a high degree of correlation between the phenotypes and genotypes of TGFBI-linked corneal dystrophies. R124 represents a mutational hotspot in the TGFBI gene. Gene mutation analysis provides a reliable basis for the definitive diagnosis of corneal dystrophy.
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Siner, Joshua, Christian Furlan Freguia, Michael Maiden, Jianhua Liu, Stefano Baila, and Valder Arruda. "Protease-Activated Receptor 4 (PAR4) Plays a Critical Role in Fetal Loss and Peripheral Thrombosis in a Mouse Model of Thrombophilia." Blood 118, no. 21 (November 18, 2011): 373. http://dx.doi.org/10.1182/blood.v118.21.373.373.

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Abstract Abstract 373 We generated a mouse model of thrombophilia by combining two common risk factors for thrombosis in humans; transgenic for high levels of FIX (TgFIX+) and activated protein C resistance due to factor V Leiden mutation (FVLQ). Breedings were used in which both parents were heterozygous for the FVL (FVLR/Q) mutation, but only one carried the TgFIX+(resulting in ∼5-fold higher of normal levels). More than 200 newborns were obtained but surprisingly no animal of FVLQ/Q/ TgFIX+ genotype was identified. When pregnancies were interrupted at embryonic age of E9.5 to E16.5, no deviation from the expected/observed embryo genotypes ratios was observed. However, the number of reabsorbed embryos increased significantly from 13% (E9.5) to 33% (E.16.5), p<0.02. All FVLQ/Q/ TgFIX+ embryos exhibited findings consistent with disseminated intravascular coagulation. Placental analysis (n=18) of these embryos harvested at E12.5 or later demonstrated prothrombotic abnormalities such as excessive fibrin deposition and innumerous apoptotic cells, determined by TUNEL assay, localized mainly in the labyrinthine trophoblast zone. The maternal genotype clearly influenced the pregnancy outcome since the number of newborns per litter was 2-fold lower when the mother carried the TgFIX+versus the paternal (average 4.3 vs. 8.3, respectively; p<0.02). No other genotypes analyzed (n=112) presented similar abnormalities in either embryos or in placental tissue. Maternal anticoagulant therapy with heparin or specific thrombin or factor Xa inhibitors reverted the prothrombotic placental phenotype, although a few newborns reached to term, none survived beyond day 1. Although FVLR/Q/ TgFIX+mice developed normally when reaching 8–10 months of age we observed a high rate of spontaneous peripheral thrombotic episodes (3/40; 7.5%) and histological analysis confirmed venous thrombosis. Thus, these mice represent a novel murine model of venous thrombosis. Moreover, this complication was also present in 5.2% of the FVLR/R/ TgFIX+ whereas no other age-matched mice (n=74) developed such complications. There was an age-dependent increase in TAT and D-Dimer levels in both prothrombotic strains by comparing samples collected at 2 and 10 months time points. In the FVLR/Q/ TgFIX+ or FVLR/R/ TgFIX+, levels of TAT (70ng/ml, n=28/group) and D-dimers (230ng/ml, n=17/group) were ∼ 2-fold higher (P<0.04), when compared to mice (TAT: 30ng/ml and D-Dimer: 100ng/ml) of other genotypes. Similarly, the highest fibrin deposition determined by Western blot analysis of tissues harvested was found in the FVLR/Q/ TgFIX+ followed by FVLR/R/ TgFIX+ mice when compared to the other animals (P<0.05). Thus, this model provides a unique opportunity to test the effect of modulators of thrombosis in a chronic thrombophilia status rather than simply upon chemical- or laser-induced acute vascular injury. Since thrombin-mediated mouse platelet activation is PAR4 dependent in an acute vascular injury model, we sought to determine whether PAR4 could modulate the prothrombotic phenotype in our chronic thrombophilia model. Using triallelic crosses FVLQ/Q/TgFIX+/PAR4(−/−) and FVLQ/Q/TgFIX+/PAR4(+/−) animals were generated. Interestingly, we were able to rescue the fetal mortality of FVLQ/Q/ TgFIX+by introducing just one PAR4 null allele. Notably, PAR4 deficiency in heterozygous or homozygous mice of FVLQ/Q/ TgFIX+allowed them to reach term and develop normally. Kaplan-Meier analysis of both FVLQ/Q/TgFIX+/PAR4(−/−)and FVLQ/Q/TgFIX+/PAR4(+/−)mice showed survival rates of 87.5% and 65%, respectively, at the 10-month time point (ongoing observation). Notably, these rescued mice showed no evidence of peripheral thrombosis. In conclusion, we have characterized a mouse model of chronic hypercoagulability and have shown that in this model PAR4 plays a central role in modulating thrombophilic complications. Disclosures: No relevant conflicts of interest to declare.
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Runager, Kasper, Jan J. Enghild, and Gordon K. Klintworth. "Focus on molecules: Transforming growth factor beta induced protein (TGFBIp)." Experimental Eye Research 87, no. 4 (October 2008): 298–99. http://dx.doi.org/10.1016/j.exer.2007.12.001.

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37

Lee, Bong-Seon, Eonmi Kim, Hyukjae Choi, and Jong-Sup Bae. "Suppressive functions of collismycin C in TGFBIp-mediated septic responses." Journal of Natural Medicines 74, no. 2 (November 23, 2019): 387–98. http://dx.doi.org/10.1007/s11418-019-01374-9.

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38

Zhao, Min, Zhiying Su, Shiyang Zhang, Liangjin Zhuang, Yudi Xie, and Xiaodong Li. "Suppressive Role of MicroRNA-148a in Cell Proliferation and Invasion in Ovarian Cancer Through Targeting Transforming Growth Factor-β-Induced 2." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 24, no. 5 (September 14, 2016): 353–60. http://dx.doi.org/10.3727/096504016x14685034103275.

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Ovarian cancer (OC) is one of the most common gynecological malignancies. MicroRNAs (miRs) play a crucial role in the development and progression of OC, but the underlying mechanism remains largely unclear. Our study investigated the regulatory role of miR-148a in OC cell proliferation and invasion. We found that miR-148a was significantly downregulated in OC tissues compared to their matched adjacent nontumor tissues. In addition, its expression was also reduced in OC cell lines (SKOV3, ES-2, OVCAR, and A2780) compared to normal ovarian epithelial cells. Overexpression of miR-148a caused a significant decrease in OC cell proliferation and invasion, as well as reduced MMP9 protein levels. Transforming growth factor-β-induced 2 (TGFI2) was further identified as a target gene of miR-148a, and its protein expression was downregulated in OC cells after miR-148a overexpression. Restoration of TGFI2 attenuated the suppressive effects of miR-148a on OC cell proliferation and invasion. Moreover, we found that TGFI2 was remarkably upregulated in OC tissues when compared with their matched adjacent nontumor tissues, and observed a reverse correlation between miR-148a and TGFI2 expression in OC tissues. On the basis of these findings, we suggest that miR-148a inhibits OC cell proliferation and invasion partly through inhibition of TGFI2. Therefore, our study highlights the importance of the miR-148a/TGFI2 axis in the malignant progression of OC.
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Foltz, Jennifer, Jena Moseman, Aarohi Thakkar, Nitin Chakravarti, and Dean Lee. "TGFβ Imprinting During Activation Promotes Natural Killer Cell Cytokine Hypersecretion." Cancers 10, no. 11 (November 5, 2018): 423. http://dx.doi.org/10.3390/cancers10110423.

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Transforming growth factor-beta (TGFβ) is a potent immunosuppressive cytokine that inhibits the anti-tumor responses of NK cells and T cells. However, the stimulation of natural killer (NK) cells with pro-inflammatory cytokines decreases NK cell sensitivity to TGFβ. Herein, we sought to determine if TGFβ imprinting (TGFβi) during NK cell activation and expansion would decrease NK cell sensitivity to TGFβ suppression. To this end, we demonstrate that the activation of NK cells during chronic IL-2 stimulation and TGFβi potently induces NK cell hypersecretion of interferon-gamma (IFNγ) and tumor necrosis factor-alpha (TNFα) in response to tumor targets which persists for at least one month in vitro after the removal of TGFβ. TGFβi NK cell cytokine hypersecretion is induced following both cytokine and tumor activation. Further, TGFβi NK cells have a marked suppression of SMAD3 and T-bet which is associated with altered chromatin accessibility. In contrast to their heightened cytokine secretion, TGFβi NK cells downregulate several activating receptors, granzyme and perforin, and upregulate TRAIL, leading to cell-line-specific alterations in cytotoxicity. These findings may impact our understanding of how TGFβ affects NK cell development and anti-tumor function.
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Guan, Yao-Zong, Hao Liu, Huan-Jie Huang, Dong-Yan Liang, Si-Ying Wu, and Tang Zhang. "Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation." Computational and Mathematical Methods in Medicine 2022 (November 8, 2022): 1–14. http://dx.doi.org/10.1155/2022/1643674.

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Background. Transforming growth factor beta-induced protein (TGFBI, encoded by TGFBI gene), is an extracellular matrix protein, widely expressed in variety of tissues. It binds to collagens type I, II, and IV and plays important roles in the interactions of cell with cell, collagen, and matrix. It has been reported to be associated with myocardial fibrosis, and the latter is an important pathophysiologyical basis of atrial fibrillation (AF). However, the mechanism of TGFBI in AF remains unclear. We aimed to detect the potential mechanism of TGFBI in AF via bioinformatics analysis. Methods. The microarray dataset of GSE115574 was examined to detect the genes coexpressed with TGFBI from 14 left atrial tissue samples of AF patients. TGFBI coexpression genes were then screened using the R package. Using online analytical tools, we determined the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, Gene Ontology (GO) annotation, and protein-protein interaction (PPI) network of TGFBI and its coexpression genes. The modules and hub genes of the PPI-network were then identified. Another dataset, GSE79768 was examined to verify the hub genes. DrugBank was used to detect the potential target drugs. Results. In GSE115574 dataset, a total of 1818 coexpression genes (769 positive and 1049 negative) were identified, enriched in 120 biological processes (BP), 38 cellular components (CC), 36 molecular functions (MF), and 39 KEGG pathways. A PPI-network with average 12.2-degree nodes was constructed. The genes clustered in the top module constructed from this network mainly play a role in PI3K-Akt signaling pathway, viral myocarditis, inflammatory bowel disease, and platelet activation. CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 were identified and finally verified as the hub genes, mainly enriched in pathways like leukocyte transendothelial migration, PI3K-Akt signaling pathway, viral myocarditis, rheumatoid arthritis, and platelet activation. Pegcetacoplan, ocriplasmin, and carvedilol were the potential target drugs. Conclusions. We used microdataset to identify the potential functions and mechanisms of the TGFBI and its coexpression genes in AF patients. Our findings suggest that CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 may be the hub genes.
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Lang, Kerstin, Selcan Kahveci, Nadine Bonberg, Katharina Wichert, Thomas Behrens, Jan Hovanec, Florian Roghmann, et al. "TGFBI Protein Is Increased in the Urine of Patients with High-Grade Urothelial Carcinomas, and Promotes Cell Proliferation and Migration." International Journal of Molecular Sciences 20, no. 18 (September 11, 2019): 4483. http://dx.doi.org/10.3390/ijms20184483.

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Here, we discovered TGFBI as a new urinary biomarker for muscle invasive and high-grade urothelial carcinoma (UC). After biomarker identification using antibody arrays, results were verified in urine samples from a study population consisting of 303 patients with UC, and 128 urological and 58 population controls. The analyses of possible modifying factors (age, sex, smoking status, urinary leukocytes and erythrocytes, and history of UC) were calculated by multiple logistic regression. Additionally, we performed knockdown experiments with TGFBI siRNA in bladder cancer cells and investigated the effects on proliferation and migration by wound closure assays and BrdU cell cycle analysis. TGFBI concentrations in urine are generally increased in patients with UC when compared to urological and population controls (1321.0 versus 701.3 and 475.6 pg/mg creatinine, respectively). However, significantly increased TGFBI was predominantly found in muscle invasive (14,411.7 pg/mg creatinine), high-grade (8190.7 pg/mg) and de novo UC (1856.7 pg/mg; all p < 0.0001). Knockdown experiments in vitro led to a significant decline of cell proliferation and migration. In summary, our results suggest a critical role of TGFBI in UC tumorigenesis and particularly in high-risk UC patients with poor prognosis and an elevated risk of progression on the molecular level.
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Sahni, Malika, Regina Raz, J. Douglas Coffin, David Levy, and Claudio Basilico. "STAT1 mediates the increased apoptosis and reduced chondrocyte proliferation in mice overexpressing FGF2." Development 128, no. 11 (June 1, 2001): 2119–29. http://dx.doi.org/10.1242/dev.128.11.2119.

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Unregulated FGF receptor signaling results in bone malformations that affect both endochondral and intramembranous ossification, and is the basis for several genetic forms of human dwarfism. FGF signaling inhibits chondrocyte proliferation and we have previously shown that the transcription factor STAT1 mediates the growth inhibitory effect of FGF in vitro. We provide genetic evidence that STAT1 is a modulator of the negative regulation of bone growth by FGF in vivo. We crossed Stat1−/− mice with a transgenic mouse line overexpressing human FGF2 (TgFGF). TgFGF mice exhibit phenotypes characterized by chondrodysplasia and macrocephaly, which affect endochondral and intramembranous ossification. We found that the chondrodysplasic phenotype of these mice results both from reduced proliferation and increased apoptosis of growth plate chondrocytes. Loss of STAT1 function in TgFGF mice led to a significant correction of the chondrodysplasic phenotype, but did not affect the skull malformations. The reduced proliferation of TgFGF growth plate chondrocytes, as well as their excessive apoptosis, were restored to near-normal levels in the absence of STAT1 function. Unregulated FGF signaling in TgFGF mice also induced apoptosis in calvarial osteoblasts that was not, however, corrected by the absence of STAT1. Detailed analysis of Stat1−/− growth plates uncovered a transient phenotype, characterized by an expansion of the proliferative zone and by acceleration of longitudinal bone growth, that attenuated as the animals grew older. These results document an essential role for STAT1 in FGF-mediated regulation of cell growth that is specific to the epiphyseal growth plate.
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Iwafuchi, Yoichi, Tetsuo Morioka, Yuko Oyama, Kandai Nozu, Kazumoto Iijima, and Ichiei Narita. "A Case of Transforming Growth Factor-β-Induced Gene-Related Oculorenal Syndrome: Granular Corneal Dystrophy Type II with a Unique Nephropathy." Case Reports in Nephrology and Dialysis 6, no. 3 (September 13, 2016): 106–13. http://dx.doi.org/10.1159/000449129.

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Many types of inherited renal diseases have ocular features that occasionally support a diagnosis. The following study describes an unusual example of a 40-year-old woman with granular corneal dystrophy type II complicated by renal involvement. These two conditions may coincidentally coexist; however, there are some reports that demonstrate an association between renal involvement and granular corneal dystrophy type II. Granular corneal dystrophy type II is caused by a mutation in the transforming growth factor-β-induced (TGFBI) gene. The patient was referred to us because of the presence of mild proteinuria without hematuria that was subsequently suggested to be granular corneal dystrophy type II. A kidney biopsy revealed various glomerular and tubular basement membrane changes and widening of the subendothelial space of the glomerular basement membrane by electron microscopy. However, next-generation sequencing revealed that she had no mutation in a gene that is known to be associated with monogenic kidney diseases. Conversely, real-time polymerase chain reaction, using a simple buccal swab, revealed TGFBI heteromutation (R124H). The TGFBI protein plays an important role in cell-collagen signaling interactions, including extracellular matrix proteins which compose the renal basement membrane. This mutation can present not only as corneal dystrophy but also as renal disease. TGFBI-related oculorenal syndrome may have been unrecognized. It is difficult to diagnose this condition without renal electron microscopic studies. To the best of our knowledge, this is the first detailed report of nephropathy associated with a TGFBI mutation.
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Choi, Seung-Il, Bong-Yoon Kim, Shorafidinkhuja Dadakhujaev, James V. Jester, Hyunmi Ryu, Tae-im Kim, and Eung Kweon Kim. "Inhibition of TGFBIp Expression by Lithium: Implications forTGFBI-Linked Corneal Dystrophy Therapy." Investigative Opthalmology & Visual Science 52, no. 6 (May 17, 2011): 3293. http://dx.doi.org/10.1167/iovs.10-6405.

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45

Thapa, Narendra, Byung-Heon Lee, and In-San Kim. "TGFBIp/βig-h3 protein: A versatile matrix molecule induced by TGF-β." International Journal of Biochemistry & Cell Biology 39, no. 12 (2007): 2183–94. http://dx.doi.org/10.1016/j.biocel.2007.06.004.

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46

Lee, Wonhwa, Sae-Kwang Ku, and Jong-Sup Bae. "Ameliorative Effect of Vicenin-2 and Scolymoside on TGFBIp-Induced Septic Responses." Inflammation 38, no. 6 (June 18, 2015): 2166–77. http://dx.doi.org/10.1007/s10753-015-0199-9.

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47

Piao, Mz, Xt Zhou, Lc Wu, and Ry Chu. "Arg555Gln Mutation of TGFBI Gene in Geographical-Type Reis—Bücklers Corneal Dystrophy in a Chinese Family." Journal of International Medical Research 40, no. 3 (June 2012): 1149–55. http://dx.doi.org/10.1177/147323001204000335.

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OBJECTIVE: Mutations of the transforming growth factor β-induced ( TGFBI) gene were studied in a Chinese family with Reis—Bücklers corneal dystrophy (RBCD). METHODS: Six family members with RBCD and six unaffected family members were investigated. The pedigree showed a typical dominant inheritance pattern. Genomic DNA was extracted from peripheral leucocytes from all study participants. Exons 4, 12 and 14 of the TGFBI gene were analysed using polymerase chain reaction, and standard automated sequencing was performed. Corneal tissue sampled from the proband during phototherapeutic keratectomy was examined using transmission electron microscopy (TEM). RESULTS: A typical geographical pattern of fine opacities in Bowman's layer of the cornea was seen in all six patients on slit-lamp examination. An Arg555Gln (R555Q) mutation of the TGFBI gene was identified in all six patients but was absent in all unaffected family members. TEM revealed rod-shaped bodies in Bowman's layer of the cornea. CONCLUSIONS: In this Chinese family an R555Q mutation of the TGFBI gene was associated with RBCD. As the RBCD phenotype is usually associated with an R124L mutation, this novel genotype—phenotype correlation may prompt further investigation of Bowman's layer corneal dystrophy.
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48

Shang, Donghao, Gang Li, Caixing Zhang, and Yuting Liu. "Synergistic inhibitory effects of 5-aza-2′-deoxycytidine and cisplatin on urothelial carcinoma growth via suppression of TGFBI-MAPK signaling pathways." Biochemistry and Cell Biology 100, no. 2 (April 2022): 115–24. http://dx.doi.org/10.1139/bcb-2021-0277.

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This study aimed to reveal the gene transcriptional alterations, possible molecular mechanisms, and pathways involved in the synergy of 5-aza-2′-deoxycytidine (DAC) and Cisplatin (CDDP) in urothelial carcinoma (UC). Two UC cell lines, 5637 and T24, were used in the present study. A cDNA microarray was performed to identify critical genes involved in the synergistic mechanism of both agents against UC cells. The results showed that several key regulatory genes, such as interleukin 24 (IL24), fibroblast growth factor 1 (FGF1), and transforming growth factor beta induced (TGFBI), may play critical roles in the synergy of DAC and CDDP in UC. Pathway enrichment suggested that many carcinogenesis-related pathways, such as the ECM-receptor interaction and MAPK signaling pathways, may participate in the synergy of both agents. Our results suggest that TGF-β1 stimulates the phosphorylation of ERK1/2 and p38 by increasing TGFBI expression, and that the TGFBI-MAPK signaling pathway plays an important role in the synergy of DAC and CDDP against UC. Therefore, we revealed the synergistic mechanism of DAC and CDDP in UC. Several key regulatory genes play critical roles in the synergy of combined treatment, and the TGFBI-MAPK signaling pathway may be an important potential target of these two agents.
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49

Ji, Yong Woo, Hyunmin Ahn, Kyoung-Jin Shin, Tae-im Kim, Kyoung Yul Seo, R. Doyle Stulting, and Eung Kweon Kim. "De Novo L509P Mutation of the TGFBI Gene Associated with Slit-Lamp Findings of Lattice Corneal Dystrophy Type IIIA." Journal of Clinical Medicine 11, no. 11 (May 28, 2022): 3055. http://dx.doi.org/10.3390/jcm11113055.

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Background: Mutations of the transforming growth factor-β-induced (TGFBI) gene produce various types of corneal dystrophy. Here, we report a novel de novo L509P mutation not located in a known hot spot of the transforming growth factor-β-induced (TGFBI) gene and its clinical phenotype, which resembles that of lattice corneal dystrophy type IIIA (LCD IIIA). Case presentation: A 36-year-old man (proband) visited our clinic due to decreased visual acuity with intermittent ocular irritation in conjunction with painful recurrent erosions in both eyes for 10 years. Molecular genetic analyses revealed a TGFBI L509P mutation (c.1526T>C) in the proband and one of his sons. Interestingly, neither TGFBI mutations nor corneal abnormalities were detected in either of the proband’s biological parents, indicating the occurrence of a de novo L509P mutation. Clinical examinations, including slit-lamp retro-illumination and Fourier-domain anterior segment optical coherence tomography (FD-OCT), revealed gray deposits in the anterior stroma and deeper refractile lines extending from limbus to limbus in both corneas of the proband, consistent with a diagnosis of LCD IIIA. Superficial diffuse haze and surface irregularity were observed in conjunction with corneal erosions and visual impairment, necessitating phototherapeutic keratectomy (PTK). A 60 μm PTK of the Bowman layer and anterior stroma of the proband’s left eye was performed following the removal of the epithelium in order to remove superficial corneal opacities. His BCVA improved from 20/400 to 20/50 at postoperative week 8 and was maintained for 45 months. Pinhole-corrected VA was 20/20 at the last visit, and corneal opacities had not recurred. Conclusions: An inheritable de novo mutation of L509P in the TGFBI gene can produce severe LCD IIIA, which can be successfully treated with OCT-guided PRK.
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Yeh, Liang-Tsai, Chiao-Wen Lin, Ko-Hsiu Lu, Yi-Hsien Hsieh, Chao-Bin Yeh, Shun-Fa Yang, and Jia-Sin Yang. "Niclosamide Suppresses Migration and Invasion of Human Osteosarcoma Cells by Repressing TGFBI Expression via the ERK Signaling Pathway." International Journal of Molecular Sciences 23, no. 1 (January 1, 2022): 484. http://dx.doi.org/10.3390/ijms23010484.

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Osteosarcoma is a highly common malignant bone tumor. Its highly metastatic properties are the leading cause of mortality for cancer. Niclosamide, a salicylanilide derivative, is an oral antihelminthic drug of known anticancer potential. However, the effect of niclosamide on osteosarcoma cell migration, invasion and the mechanisms underlying have not been fully clarified. Therefore, this study investigated niclosamide’s underlying pathways and antimetastatic effects on osteosarcoma. In this study, U2OS and HOS osteosarcoma cell lines were treated with niclosamide and then subjected to assays for determining cell migration ability. The results indicated that niclosamide, at concentrations of up to 200 nM, inhibited the migration and invasion of human osteosarcoma U2OS and HOS cells and repressed the transforming growth factor beta-induced protein (TGFBI) expression of U2OS cells, without cytotoxicity. After TGFBI knockdown occurred, cellular migration and invasion behaviors of U2OS cells were significantly reduced. Moreover, niclosamide significantly decreased the phosphorylation of ERK1/2 in U2OS cells and the combination treatment of the MEK inhibitor (U0126) and niclosamide resulted in the intensive inhibition of the TGFBI expression and the migratory ability in U2OS cells. Therefore, TGFBI derived from osteosarcoma cells via the ERK pathway contributed to cellular migration and invasion and niclosamide inhibited these processes. These findings indicate that niclosamide may be a powerful preventive agent against the development and metastasis of osteosarcoma.
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