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Littérature scientifique sur le sujet « Mammary gland involution »

Auteur : Grafiati

Publié le 10 mars 2023

Mis à jour le 22 juin 2025

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Articles de revues sur le sujet "Mammary gland involution"

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Dickson, S. R., and M. J. Warburton. "Enhanced synthesis of gelatinase and stromelysin by myoepithelial cells during involution of the rat mammary gland." Journal of Histochemistry & Cytochemistry 40, no. 5 (1992): 697–703. http://dx.doi.org/10.1177/40.5.1315355.

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During the involution of the mammary gland there is destruction of the basement membrane as the secretory alveolar structures degenerate. Immunofluorescence staining of sections of rat mammary gland with antibodies to 72 KD gelatinase (MMP-2) and stromelysin (MMP-3) revealed increased production of these two proteinases during involution. This increased expression was mostly restricted to myoepithelial cells. Increased expression during involution was also demonstrated by immunoblotting techniques. Gelatin zymography indicated that the predominant metalloproteinase present in involuting rat mammary glands was a 66 KD gelatinase.

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Lund, L. R., S. F. Bjorn, M. D. Sternlicht, et al. "Lactational competence and involution of the mouse mammary gland require plasminogen." Development 127, no. 20 (2000): 4481–92. http://dx.doi.org/10.1242/dev.127.20.4481.

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Urokinase-type plasminogen activator expression is induced in the mouse mammary gland during development and post-lactational involution. We now show that primiparous plasminogen-deficient (Plg(−/−)) mice have seriously compromised mammary gland development and involution. All mammary glands were underdeveloped and one-quarter of the mice failed to lactate. Although the glands from lactating Plg(−/−) mice were initially smaller, they failed to involute after weaning, and in most cases they failed to support a second litter. Alveolar regression was markedly reduced and a fibrotic stroma accumulated in Plg(−/−) mice. Nevertheless, urokinase and matrix metalloproteinases (MMPs) were upregulated normally in involuting glands of Plg(−/−) mice, and fibrin did not accumulate in the glands. Heterozygous Plg(+/−) mice exhibited haploinsufficiency, with a definite, but less severe mammary phenotype. These data demonstrate a critical, dose-dependent requirement for Plg in lactational differentiation and mammary gland remodeling during involution.

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Talhouk, R. S., M. J. Bissell, and Z. Werb. "Coordinated expression of extracellular matrix-degrading proteinases and their inhibitors regulates mammary epithelial function during involution." Journal of Cell Biology 118, no. 5 (1992): 1271–82. http://dx.doi.org/10.1083/jcb.118.5.1271.

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Extracellular matrix (ECM) plays an important role in the maintenance of mammary epithelial differentiation in culture. We asked whether changes in mouse mammary specific function in vivo correlate with changes in the ECM. We showed, using expression of beta-casein as a marker, that the temporal expression of ECM-degrading proteinases and their inhibitors during lactation and involution are inversely related to functional differentiation. After a lactation period of 9 d, mammary epithelial cells maintained beta-casein expression up to 5 d of involution. Two metalloproteinases, 72-kD gelatinase (and its 62-kD active form), and stromelysin, and a serine proteinase tissue plasminogen activator were detected by day four of involution, and maintained expression until at least day 10. The expression of their inhibitors, the tissue inhibitor of metalloproteinases (TIMP) and plasminogen activator inhibitor-1, preceded the onset of ECM-degrading proteinase expression and was detected by day two of involution, and showed a sharp peak of expression centered on days 4-6 of involution. When involution was accelerated by decreasing lactation to 2 d, there was an accelerated loss of beta-casein expression evident by day four and a shift in expression of ECM-remodeling proteinases and inhibitors to a focus at 2-4 d of involution. To further extend the correlation between mammary-specific function and ECM remodeling we initiated involution by sealing just one gland in an otherwise hormonally sufficient lactating animal. Alveoli in the sealed gland contained casein for at least 7 d after sealing, and closely resembled those in a lactating gland. The relative expression of TIMP in the sealed gland increased, whereas the expression of stromelysin was much lower than that of a hormone-depleted involuting gland, indicating that the higher the ratio of TIMP to ECM-degrading proteinases the slower the process of involution. To test directly the functional role of ECM-degrading proteinases in the loss of tissue-specific function we artificially perturbed the ECM-degrading proteinase-inhibitor ratio in a normally involuting gland by maintaining high concentrations of TIMP protein with the use of surgically implanted slow-release pellets. In a concentration-dependent fashion, involuting mammary glands that received TIMP implants maintained high levels of casein and delayed alveolar regression. These data suggest that the balance of ECM-degrading proteinases and their inhibitors regulates the organization of the basement membrane and the tissue-specific function of the mammary gland.(ABSTRACT TRUNCATED AT 400 WORDS)

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Tian, Lei, Shancheng Guo, Zhiye Zhao, et al. "miR-30a-3p Regulates Autophagy in the Involution of Mice Mammary Glands." International Journal of Molecular Sciences 24, no. 18 (2023): 14352. http://dx.doi.org/10.3390/ijms241814352.

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The mammary gland undergoes intensive remodeling during the lactation cycle, and the involution process of mammary gland contains extensive epithelial cells involved in the process of autophagy. Our studies of mice mammary glands suggest that miR-30a-3p expression was low during involution compared with its high expression in the mammary glands of lactating mice. Then, we revealed that miR-30a-3p negatively regulated autophagy by autophagy related 12 (Atg12) in mouse mammary gland epithelial cells (MMECs). Restoring ATG12, knocking down autophagy related 5 (Atg5), starvation, and Rapamycin were used to further confirm this conclusion. Overexpression of miR-30a-3p inhibited autophagy and altered mammary structure in the involution of the mammary glands of mice, which was indicative of alteration in mammary remodeling. Taken together, these results elucidated the molecular mechanisms of miR-30a-3p as a key induction mediator of autophagy by targeting Atg12 within the transition period between lactation and involution in mammary glands.

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Batan, Sonia, Jabunnesa Khanom, Sabarish Ramachandran, et al. "Abstract P3-04-04: The Butyrate Transporter SLC5A8 Selectively Inhibits Breast Tumor Metastasis." Clinical Cancer Research 31, no. 12_Supplement (2025): P3–04–04—P3–04–04. https://doi.org/10.1158/1557-3265.sabcs24-p3-04-04.

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Abstract Introduction: The mammary gland is a dynamic organ that undergoes significant developmental changes during pregnancy, lactation, and involution. The process of involution is a highly orchestrated series of molecular and physical events that can be divided into two distinct phases. (Lund et al., 1996). Accumulation of milk in the alveolar lumen (milk stasis) is required to initiate the first phase during which the secretory cells begin to enter apoptosis. Here we provide genetic and molecular biological evidence to shows that the short-chain fatty acid Butyrate (BTR), a significant component in milk, contributes to milk stasis-induced apoptosis in the mammary gland, and SLC5A8, a BTR transporter, is obligatory for this effect. Slc5a8 deletion in mice is associated with delayed mammary gland involution, susceptible forto chemical, xenograft, and syngeneic transplant, and predisposes to early onset of mammary tumorigenesis and accelerated lung metastasis driven by genetically engineered mouse models of breast and lung cancers. Objective: To establish the functional link between mammary gland remodeling and its relevance to mammary tumor growth (primary) and distant metastasis. Methods: All animals were housed and handled according to approved protocols established by the Georgia Health SciencesAugusta University (GHSUAU) Animal Care and Use Committee and NIH guidguidelinesance’s. For the measurement of HDAC activity, A commercially available HDAC assay kit (BioVisionBio Vision) was used. Statistical analysis was done using one-way ANOVA followed by Bonferroni multiple comparison test. The software used was Graph Pad Prism, version 5.0. A p-value &lt;0.05 was considered statistically significant. Results: SLC5A8 is a tumor suppressor, and its expression is silenced in many human cancers, including breast cancer (Thangaraju et al., 2006a; Babu et al., 2011). Here we analyzed Slc5a8 expression at various stages of mammary gland development. Slc5a8 expression was evident at mRNA and protein levels in the virgin mammary gland; it was induced marginally during pregnancy and lactation. Slc5a8 was primarily expressed in the lumen-facing apical membrane of the mammary ductal epithelium. deletion of Slc5a8 in mice leads to a delay in mammary gland involution. We also analyzed the expression of involution markers (Stat3, p53, Bax, BMF, survivin, and IGFBP-5) and apoptotic cell death in wild wild-type (Slc5a8-/-) and Slc5a8-knockout (Slc5a8-/-) mice mammary glands at different stages of involution. pStat3 expression was increased dramatically on Inv d1 and d2 in wild- type glands but to a much less extent in Slc5a8 -/- glands. Further, the expression of p53 and Bax (pro-apoptotic genes), BMF (anoikis inducer), and IGFBP-5 (inhibitor of IGF-induced prosurvival signaling) were significantly increased in wild wild-type glands compared to Slc5a8-/- glands. The anti-apoptotic protein survivin was significantly reduced on Inv d1, d2, and d3 in wild wild-type glands, but this reduction was not observed in Slc5a8-/- glands. Slc5a8 transports into cells the HDAC inhibitors butyrate, pyruvate, and propionate into cells the. (Thangaraju et al., 2009). These inhibitors are selective for HDAC1 and HDAC3. Butyrate, a significant component of breast milk, promotes differentiation in normal cells but induces apoptosis in highly proliferative cells and cancer cells. Slc5a8 induces apoptosis in lactating mammary epithelial cells during involution through modulation of HDAC expression and activity. Butyrate, a substrate of Slc5a8, plays a critical role in promoting mammary gland involution through HDAC inhibition and death receptor activation. Administration of exogenous butyrate induces precocious mammary gland involution in mice. Next, we wanted to exploretested whether if the deletion of Slc5a8 plays any a role in mammary tumorigenesis. The biological changes that occur in mammary epithelial cells during pregnancy/lactation and involution are similar in many respects to those associated with tumor development and tumor regression, respectively. Deletion of Slc5a8 in mice is associated with early onset of mammary tumor formation, accelerated lung metastasis, and decreased overall survival. Finally, we wanted to analyze whether if mammary gland-specific overexpression of Slc5a8 SLC5A8 would influence mammary gland involution and mammary tumorigenesis. Mammary gland-specific overexpression of Slc5a8 SLC5A8 induces precocious mammary gland involution and protects from MMTV-Neu-driven mammary tumorigenesis. Conclusion: Slc5a8 is a tumor suppressor in the mammary gland, and butyrate is essential for its tumor-suppressive function. Mammary gland-selective overexpression of Slc5a8 SLC5A8 in mice enhances mammary gland involution and protects against breast cancer. Citation Format: Sonia Batan, Jabunnesa Khanom, Sabarish Ramachandran, Selvakumar Elangovan, Nanditi N. Thangaraju, Subha Sundaram, Snigdha Ganjikunta, Breanna Kennedy, Vadivel Ganapathy, Puttur D. Prasad, Muthusamy Thangaraju. The Butyrate Transporter SLC5A8 Selectively Inhibits Breast Tumor Metastasis [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2024; 2024 Dec 10-13; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(12 Suppl):Abstract nr P3-04-04.

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Schwertfeger, Kathryn L., Monica M. Richert, and Steven M. Anderson. "Mammary Gland Involution Is Delayed by Activated Akt in Transgenic Mice." Molecular Endocrinology 15, no. 6 (2001): 867–81. http://dx.doi.org/10.1210/mend.15.6.0663.

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Abstract Activation of the antiapoptotic protein kinase Akt is induced by a number of growth factors that regulate mammary gland development. Akt is expressed during mammary gland development, and expression decreases at the onset of involution. To address Akt actions in mammary gland development, transgenic mice were generated expressing constitutively active Akt in the mammary gland under the control of the mouse mammary tumor virus (MMTV) promoter. Analysis of mammary glands from these mice reveals a delay in both involution and the onset of apoptosis. Expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), an inhibitor of matrix metalloproteinases (MMPs), is prolonged and increased in the transgenic mice, suggesting that disruption of the MMP:TIMP ratio may contribute to the delayed mammary gland involution observed in the transgenic mice.

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Bernhardt, Sarah M., and Pepper Schedin. "Abstract B011: The anti-cancer effects of vitamin D are blocked postpartum, due to suppression of vitamin D metabolism in the involuting liver." Cancer Prevention Research 15, no. 12_Supplement_1 (2022): B011. http://dx.doi.org/10.1158/1940-6215.dcis22-b011.

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Abstract Postpartum mammary gland involution is a physiologic window of increased breast cancer risk. It has been proposed that the poor prognosis associated with postpartum breast cancer is due to the involuting mammary microenvironment promoting progression of indolent lesions to invasive disease. As such, the involuting gland has been implicated as a target for preventive strategies. Vitamin D has anti-cancer properties, and there are data demonstrating that vitamin D supplementation protects against breast cancer progression in mouse models. Moreover, vitamin D deficiency is prevalent in postpartum women, suggesting that vitamin D supplementation during the vitamin D-deficient, at-risk window of involution may be an approach for preventing the progression of indolent lesions. Here, we characterized how vitamin D deficiency and supplementation affect tumor growth in a mouse model of postpartum breast cancer. Vitamin D deficiency and sufficiency were established in BALB/c mice through feeding diets containing low or high levels of vitamin D. Quantification of serum 25(OH)D verified that diets resulted in vitamin D deficiency (25.8±4.3nmol/L;mean±stdev) or sufficiency (66.4±11.7nmol/L) at levels comparable to humans. Murine mammary cancer cells (D2A1, 2×104 cells, 20µL) were injected into mammary fatpads of involuting (2 days post wean), or age-matched nulliparous mice (n=5-12 mice/group), and tumor growth tracked for 4 weeks. Independent of vitamin D status, tumors exposed to the involuting mammary gland grew 1.8-fold larger than tumors exposed to the nulliparous gland (p&lt;0.001); consistent with prior data showing that the microenvironment of the involuting gland is tumor promotional. Interestingly, while vitamin D supplementation of nulliparous mice associated with a 3.4-fold reduction in tumor growth (p=0.03), vitamin D supplementation of involution mice did not reduce tumor growth. Dietary vitamin D is metabolized to its active form in the liver. Our group has previously shown that the liver also undergoes weaning-induced involution. Thus, we tested if involution of the liver impairs metabolism of vitamin D to its active form, potentially contributing to the null effects of vitamin D supplementation in involution mice. We collected serum from mice on vitamin D deficient and supplemented diets across reproductive time points (nulliparous, lactation, involution days 2, 4, 6), and found that vitamin D supplementation during involution was insufficient to restore serum vitamin D to levels of sufficiency. Further, gene expression analysis of livers show that expression of Cyp2r1 and Cyp27a1—genes involved in vitamin D activation—were reduced during involution. Together, these findings suggest that impaired metabolism of vitamin D during involution may reduce the availability of active vitamin D, and contribute to the null effect observed in involution mice. Understanding the mechanisms by which mammary gland involution influences the anti-cancer effects of vitamin D is required to optimize cancer prevention strategies that target this window. Citation Format: Sarah M Bernhardt, Pepper Schedin. The anti-cancer effects of vitamin D are blocked postpartum, due to suppression of vitamin D metabolism in the involuting liver [abstract]. In: Proceedings of the AACR Special Conference on Rethinking DCIS: An Opportunity for Prevention?; 2022 Sep 8-11; Philadelphia, PA. Philadelphia (PA): AACR; Can Prev Res 2022;15(12 Suppl_1): Abstract nr B011.

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Jena, Manoj Kumar, and Ashok Kumar Mohanty. "NEW INSIGHTS OF MAMMARY GLAND DURING DIFFERENT STAGES OF DEVELOPMENT." Asian Journal of Pharmaceutical and Clinical Research 10, no. 11 (2017): 35. http://dx.doi.org/10.22159/ajpcr.2017.v10i11.20801.

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Mammary gland is a unique organ with its function of milk synthesis, secretion, and involution to prepare the gland for subsequent lactation. The mammary epithelial cells proliferate, differentiate, undergo apoptosis, and tissue remodeling following a cyclic pathway in lactation – involution – lactation cycle, thus fine tuning the molecular events through hormones, and regulatory molecules. Several studies are performed on the mammary gland development, lactogenesis, and involution process in molecular details. The developmental stages of mammary gland are embryonic, pre-pubertal, pubertal, pregnancy, lactation, and involution. Major developmental processes occur after puberty with hormones and growth factors playing crucial role. The two major pathways such as Janus kinases-signal transducer and activator of transcription pathway and PI3K-Akt pathway play a major role in maintaining the lactation. The involution process is a well-orchestrated event involving several signaling molecules and making the gland ready for subsequent lactation. The review focuses on findings with molecular details of different stages of the mammary gland development and signaling pathways involved in lactation–involution cycle. Deep insight into the developmental stages of mammary gland will pave the way to understand mammary gland biology, apoptosis, oncogenesis, and it will help the researchers to use mammary gland as a model for research on various aspects.

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Atabai, Kamran, Rafael Fernandez, Xiaozhu Huang, et al. "Mfge8 Is Critical for Mammary Gland Remodeling during Involution." Molecular Biology of the Cell 16, no. 12 (2005): 5528–37. http://dx.doi.org/10.1091/mbc.e05-02-0128.

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Apoptosis is a critical process in normal mammary gland development and the rapid clearance of apoptotic cells prevents tissue injury associated with the release of intracellular antigens from dying cells. Milk fat globule-EGF-factor 8 (Mfge8) is a milk glycoprotein that is abundantly expressed in the mammary gland epithelium and has been shown to facilitate the clearance of apoptotic lymphocytes by splenic macrophages. We report that mice with disruption of Mfge8 had normal mammary gland development until involution. However, abnormal mammary gland remodeling was observed postlactation in Mfge8 mutant mice. During early involution, Mfge8 mutant mice had increased numbers of apoptotic cells within the mammary gland associated with a delay in alveolar collapse and fat cell repopulation. As involution progressed, Mfge8 mutants developed inflammation as assessed by CD45 and CD11b staining of mammary gland tissue sections. With additional pregnancies, Mfge8 mutant mice developed progressive dilatation of the mammary gland ductal network. These data demonstrate that Mfge8 regulates the clearance of apoptotic epithelial cells during mammary gland involution and that the absence of Mfge8 leads to inflammation and abnormal mammary gland remodeling.

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Rivera, Olivia C., Stephen R. Hennigar, and Shannon L. Kelleher. "ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 2 (2018): R323—R335. http://dx.doi.org/10.1152/ajpregu.00444.2017.

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Mammary gland involution, a tightly regulated process of tissue remodeling by which a lactating mammary gland reverts to the prepregnant state, is characterized by the most profound example of regulated epithelial cell death in normal tissue. Defects in the execution of involution are associated with lactation failure and breast cancer. Initiation of mammary gland involution requires upregulation of lysosome biogenesis and acidification to activate lysosome-mediated cell death; however, specific mediators of this initial phase of involution are not well described. Zinc transporter 2 [ZnT2 ( SLC30A2)] has been implicated in lysosome biogenesis and lysosome-mediated cell death during involution; however, the direct role of ZnT2 in this process has not been elucidated. Here we showed that ZnT2-null mice had impaired alveolar regression and reduced activation of the involution marker phosphorylated Stat3, indicating insufficient initiation of mammary gland remodeling during involution. Moreover, we found that the loss of ZnT2 inhibited assembly of the proton transporter vacuolar ATPase on lysosomes, thereby decreasing lysosome abundance and size. Studies in cultured mammary epithelial cells revealed that while the involution signal TNFα promoted lysosome biogenesis and acidification, attenuation of ZnT2 impaired the lysosome response to this involution signal, which was not a consequence of cytoplasmic Zn accumulation. Our findings establish ZnT2 as a novel regulator of vacuolar ATPase assembly, driving lysosome biogenesis, acidification, and tissue remodeling during the initiation of mammary gland involution.

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Thèses sur le sujet "Mammary gland involution"

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Hughes, Katherine. "Inflammation and remodelling in mammary gland involution." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607688.

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Kreuzaler, Peter Anton. "Cell death modalities in mammary gland involution." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609378.

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Treisman, Loren Lee. "The role of the PARbZips in mammary gland involution." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614361.

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Charifou, Elsa. "Characterization and impact of cellular senescence during mammary gland involution." Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS559V2.pdf.

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La sénescence est une réponse à un stress biologique, caractérisée par un arrêt stable du cycle cellulaire. Néanmoins, les cellules restent métabolliquement actives et acquièrent un phenotype sécrétoire associé à la sénescence, avec la production d’un sécrétome complexe composé de cytokines, chémiokines, facteurs de croissance et modulateurs du remodelage de la matrice extracellulaire. La sénescence est associée à de nombreux processus pathologiques, comme la tumorigénèse et le vieillessement. Cependant, où, quand et comment la sénescence contribue aux processus physiologiques reste méconnu. Pour répondre à cette question, nous avons tiré profit de la glande mammaire (GM), un organe avec une plasticité remarquable pendant le développement post-natal. L’involution de la GM est l’un des évenements majeurs de mort cellulaire et de remodelage tissulaire chez les mammifères, lorsque les cellules épithéliales produisant le lait sont éliminées et que la GM retourne à son état pré-grossesse, attendant la prochaine gestation. Au cours de ma thèse, nous avons montré que la sénescence était induite transitoirement pendant la phase irréversible de l’involution. De plus, le programme de sénescence apparaissait spécifiquement dans les cellules luminales productrices de lait et corrélait à l’expression de l’inhibiteur du cycle cellulaire p16. En parallèle, nous avons établi un nouveau modèle d’organoides pour mimer la gestation, la lactation et l’involution de la GM. Dans ce modèle ex-vivo, nous avons aussi relever la présence de cellules sénescentes strictement lors du processus d’involution. Pour évaluer l’impact biologique de la sénescence in vivo, nous avons utilisé une méthode de scellement des mamelons pour découpler les phases réversible et irréversible de l’involution. Nous avons dévoilé une association étroite entre le sevrage des hormones lactogéniques qui a lieu lors de la seconde phase d’involution, et l’induction du programme de sénescence. Pour mieux définir les rôles physiologiques de la sénescence pendant l’involution, nous avons traités des souris avec de l’ABT-263, un composé sénolytique induisant l’apoptose des cellules sénescentes. Nous avons observé une altération du remodelage tissulaire suite à l’élimination des cellules sénescentes, avec des alvéoles résiduelles plus larges et un remplissage adipocytaire retardé. De plus, dans des organoides provenant de souris transgéniques p16-3MR, nous avons éliminé les cellules sénescentes avec succès grâce à l’administration de ganciclovir, ce qui a retardé le processus d’involution. Dans leur ensemble, les modèles in vivo et ex-vivo suggèrent un rôle important de la sénescence pour moduler la phase de remodelage tissulaire dans l’involution de la GM. Enfin, le processus d’involution est intiment lié avec le cancer du sein post-partum, un cancer diagnostiqué dans les 10 ans suivant une grossesse et associé à un mauvais pronostic. Explorer comment la sénescence impacte le microenvironnement lors de l’involution pourrait ainsi fournir de nouvelles connaissances pour mieux comprendre le cancer du sein post-partum<br>Cellular senescence is a biological stress response characterized by a stable cell cycle arrest. Nonetheless, cells remain metabolically active and acquire a senescence-associated secretory phenotype (SASP), a complex secretome composed of cytokines, chemokines, growth factors, and extracellular matrix remodeling modulators. Senescence is associated with various pathological processes, such as tumorigenesis and aging. However, it is unknown when, where and how senescence contributes to physiological processes. To answer this question, we took advantage of the mammary gland (MG), an organ with remarkable plasticity throughout postnatal development. The MG involution is one of the major mammalian cell death and tissue remodeling events, when milk-producing epithelial cells are removed, and the MG returns to its pre-gestation state, resting for further pregnancy. During my Ph.D., we showed that senescence was transiently induced during the irreversible phase of involution. The senescent program occurred specifically in the alveolar milk-producing luminal cells and correlated with the expression of the cell cycle inhibitor p16. In parallel, we established a novel organoid system to mimic MG gestation, lactation, and involution. In this ex-vivo model, we also highlighted the presence of senescent cells strictly during the involution-like process. To assess the biological impact of senescence in vivo, we used a teat sealing method to uncouple the reversible and irreversible phases of involution. We unveiled a close association between the withdrawal of lactogenic hormones occurring in the second phase of involution and the induction of the senescence program. To further define the physiological roles of senescence during involution, we treated mice with ABT-263, a senolytic compound inducing apoptosis of senescent cells. Interestingly, we observed an impaired tissue remodeling upon senescence elimination, with larger remaining alveolar structures and delayed adipocyte refilling. Moreover, in organoids from transgenic p16-3MR mice, we successfully removed senescent cells with ganciclovir and delayed the involution-like process. Taken together, both in vivo and ex-vivo models suggest an essential role of senescence in modulating the tissue remodeling phase of MG involution. Importantly, the involution process is intimately associated with postpartum breast cancer (PPBC), a cancer diagnosed within 10 years following delivery with a poor prognosis. Investigating how senescence impacts the microenvironment during the involution process might provide major insights to understand PPBC

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Staniszewska, Anna Dominika. "Roles of Stat3 in mammary gland development, involution and breast cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610277.

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Anderson, Torri R. "Determination of expression of Fliz1 during involution of the mouse mammary gland." Thesis, Villanova University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1565164.

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<p> Remodeling of the mouse mammary gland is a highly coordinated process that occurs after the removal of suckling pups from the mother. Involution, or shrinking of the mammary gland, after removal of the pups has been linked to apoptotic events within the mouse mammary tissue during forced weaning. Several transcription factors are hypothesized to be involved in this process. A transcription factor known as GATA-3, which was first identified in the thymus, is also important for maintenance of various tissue types within the mouse mammary gland; its loss leads to epithelial cell detachment and eventual death. Another transcription factor known as fetal zinc liver finger protein 1, or Fliz1, has been found to regulate GATA-3 in T-cells. This interaction had not been elucidated during involution in mouse mammary tissue. I hypothesized that Fliz1 is expressed at heightened levels during mouse mammary gland involution following forced weaning of pups, and that this expression correlates with a decrease in GATA-3 levels, with increased expression of the pro-apoptotic protein BAD. Using qRT-PCR, immunoblotting and immunohistochemistry I have shown that Fliz1 is indeed expressed in involuting mouse mammary gland tissue as well as several other tissue types. However, levels of Fliz1 remain fairly constant during involution. The findings also show that Cathepsin L, a known apoptotic marker for mammary gland involution, is substantially up-regulated during the process of mammary gland involution in the mouse. The study also revealed that GATA-3 levels as hypothesized decrease substantially during the process of mouse mammary gland involution, indicating that GATA-3 is required for maintenance of the mouse mammary gland.</p>

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Marshall, Aaron. "The Biology of Mammary Gland Serotonin Synthesis and Transport." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1251229830.

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Pai, Vaibhav Prakash. "Serotonin Regulation of Mammary Gland Involution and its Role in Breast Cancer Progression." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1237565289.

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Patel, Amita. "Transcriptional regulation of cathepsin L during mouse mammary gland involution a test of STAT3 involvement /." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432835.

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Stairiker, Patricia A. "The role of L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2007. http://proquest.umi.com/pqdweb?did=1075710531&sid=3&Fmt=2&clientId=3260&RQT=309&VName=PQD.

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Livres sur le sujet "Mammary gland involution"

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Hojilla, Carlo Vincent. The role of TIMP3 in mammary gland morphogenesis, involution, inflammation, and tumourigenesis. 2006.

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Wang, Ruijia. The role of apoptosis in development of mouse mammary gland: Expression of Pl3K/AKT/bad pathway in development, diffentiation, pregnancy, lactation and involution of mouse mammary gland. 1999.

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Chapitres de livres sur le sujet "Mammary gland involution"

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Marti, Andreas, Hans Graber, Hedvika Lazar, et al. "Caspases: Decoders of Apoptotic Signals During Mammary Involution." In Biology of the Mammary Gland. Springer US, 2002. http://dx.doi.org/10.1007/0-306-46832-8_24.

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Bielke, Wolfgang, Guo Ke, Robert Strange, and Robert Friis. "Apoptosis in Mammary Gland Involution: Isolation and Characterization of Apoptosis-Specific Genes." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_5.

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Monaghan, Paul, Nina Perusinghe, and W. Howard Evans. "Dramatic Changes in Gap Junction Expression in the Mammary Gland During Pregnancy, Lactation and Involution." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_37.

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Fetherston, Catherine M., Chee Seong Lee, and Peter E. Hartmann. "Mammary Gland Defense: The Role of Colostrum, Milk and Involution Secretion." In Advances in Nutritional Research Volume 10. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0661-4_8.

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Tonner, Elizabeth, James Beattie, and David J. Flint. "Production of an Insulin-Like Growth Factor Binding Protein by the Involuting Rat Mammary Gland." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_25.

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Lloyd-Lewis, Bethan, Timothy J. Sargeant, Peter A. Kreuzaler, Henrike K. Resemann, Sara Pensa, and Christine J. Watson. "Analysis of the Involuting Mouse Mammary Gland: An In Vivo Model for Cell Death." In Methods in Molecular Biology. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6475-8_7.

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Hurley, W. L. "MAMMARY GLAND | Growth, Development, Involution." In Encyclopedia of Dairy Sciences. Elsevier, 2002. http://dx.doi.org/10.1016/b0-12-227235-8/00278-9.

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Hurley, W. L., and J. J. Loor. "Mammary Gland | Growth, Development and Involution." In Encyclopedia of Dairy Sciences. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-374407-4.00291-0.

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Loor, J. J., F. Batistel, M. Bionaz, W. L. Hurley, and E. Vargas-Bello-Pérez. "Mammary Gland: Gene Networks Controlling Development and Involution." In Reference Module in Food Science. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-818766-1.00001-5.

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Loor, J. J., F. Batistel, M. Bionaz, and W. L. Hurley. "Mammary Gland: Gene Networks Controlling Development and Involution." In Reference Module in Food Science. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-08-100596-5.00883-0.

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Actes de conférences sur le sujet "Mammary gland involution"

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Garofalo, Jennifer-Marie, Dawn Bowers, Richard Browne, Brian MacQueen, Terry Mashtare, and Patricia A. Masso-Welch. "Abstract 5460: Effects of ethanol exposure during involution on mouse mammary gland." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5460.

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Ramachandran, Sabarish, Selvakumar Elangovan, Puttur D. Prasad, Vadivel Ganapathy, and Muthusamy Thangaraju. "Abstract LB-236: Differential regulation of STAT3 in mammary gland involution as well as in mammary tumorigeneis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-236.

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Martinson, Holly, Sonail Jindal, Virginia Borges, and Pepper Schedin. "Abstract A31: Immune cell influx during postpartum mammary gland involution reveals immunosuppression and tumor promotion." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a31.

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Lyons, Traci R., Virginia F. Borges, Courtney B. Betts, et al. "Abstract B099: Postpartum mammary gland involution promotes COX-2 dependent tumor cell invasion of lymphatics." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-b099.

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Ramachandran, Sabarish, Selvakumar Elangovan, Rajneesh Pathania, Puttur Devi Prasad, Vadivel Ganapathy, and Muthusamy Thangaraju. "Abstract 18: Slc5a8 inactivation is associated with mammary gland involution delay, early onset of mammary tumorigenesis and accelerated lung metastasis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-18.

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Guo, Qiuchen, and Pepper J. Schedin. "Abstract LB-009: Collagen regulation in postpartum mammary gland involution, a novel breast cancer prevention target." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-009.

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Cook, Katherine L., Anni Warri, Rong Hu, et al. "Abstract 1667: Autophagy and unfolded protein response (UPR) signaling regulates progression of apoptosis in mammary gland involution." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1667.

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Vallone, Sabrina A., Martín García Solá, Robert D. Cardiff, et al. "Abstract 3685: Sustained Ret expression during mammary gland post-lactation induces premature involution and enhances cancer potential." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3685.

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Shinde, Neelam, Kirti Kaul, Allen Zhang, et al. "Abstract PS17-28: Abrupt involution of lactating mammary gland induces metabolic reprogramming conducive to pro-tumorigenic changes." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps17-28.

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Lyons, Traci R., Jenean O'Brien, Matthew Conklin, Patricia Keely, Virginia Borges, and Pepper Schedin. "Abstract B61: Postpartum mammary gland involution drives DCIS progression through collagen and COX-2, identifying a target for intervention." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-b61.

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Rapports d'organisations sur le sujet "Mammary gland involution"

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Cowin, Pamela. Targeting the Prometastatic Microenvironment of the Involuting Mammary Gland. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada612509.

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