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Journal articles on the topic 'Relaxin-like factor'

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Published: 4 June 2021

Last updated: 13 February 2022

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1

Bamberger, Ana-Maria, Richard Ivell, Marga Balvers, Bianca Kelp, Christoph M. Bamberger, Lutz Riethdorf, and Thomas Löning. "Relaxin-Like Factor (RLF)." International Journal of Gynecological Pathology 18, no. 2 (April 1999): 163–68. http://dx.doi.org/10.1097/00004347-199904000-00011.

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2

Ivell, R. "Biology of the relaxin-like factor (RLF)." Reviews of Reproduction 2, no. 3 (September 1, 1997): 133–38. http://dx.doi.org/10.1530/revreprod/2.3.133.

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3

Ivell, R. "Biology of the relaxin-like factor (RLF)." Reviews of Reproduction 2, no. 3 (September 1, 1997): 133–38. http://dx.doi.org/10.1530/ror.0.0020133.

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4

Büllesbach, Erika E., and Christian Schwabe. "Specific, High Affinity Relaxin-like Factor Receptors." Journal of Biological Chemistry 274, no. 32 (August 6, 1999): 22354–58. http://dx.doi.org/10.1074/jbc.274.32.22354.

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5

Büllesbach, Erika E., Richard Rhodes, Barbara Rembiesa, and Christian Schwabe. "The Relaxin-Like Factor Is a Hormone." Endocrine 10, no. 2 (1999): 167–70. http://dx.doi.org/10.1385/endo:10:2:167.

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6

Büllesbach, Erika E., and Christian Schwabe. "LGR8 Signal Activation by the Relaxin-like Factor." Journal of Biological Chemistry 280, no. 15 (February 10, 2005): 14586–90. http://dx.doi.org/10.1074/jbc.m414443200.

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7

Schwabe, Christian, and Erika E. Büllesbach. "The “Hot Wires” of the Relaxin-Like Factor (Insl3)." Annals of the New York Academy of Sciences 1160, no. 1 (April 2009): 93–98. http://dx.doi.org/10.1111/j.1749-6632.2008.03779.x.

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8

Tomboc, Marlah, Peter A. Lee, Mohamed F. Mitwally, Francis X. Schneck, Mark Bellinger, and Selma F. Witchel. "Insulin-like 3/Relaxin-Like Factor Gene Mutations Are Associated with Cryptorchidism1." Journal of Clinical Endocrinology & Metabolism 85, no. 11 (November 1, 2000): 4013–18. http://dx.doi.org/10.1210/jcem.85.11.6935.

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Cryptorchidism is a common anomaly of male sexual differentiation. Two phases of testicular descent are recognized, transabdominal and inguinoscrotal. With evidence that androgens and Müllerian inhibitory hormone were not completely responsible for testicular descent, the existence of a third testicular hormone mediating testicular descent was postulated. Insulin-like 3 (INSL3) [also known as relaxin-like factor (RLF) and Leydig insulin-like protein (LEY I-L)] is a member of the insulin/relaxin hormone superfamily that is highly expressed in Leydig cells. The phenotype of transgenic mice with targeted deletion of the Insl3 gene was bilateral cryptorchidism with morphological evidence of abnormal gubernacular development. With this implicit evidence that Insl3 mediates testicular descent in mice, we performed mutation detection analysis of the coding regions of the 2 exon INSL3 gene in genomic DNA samples obtained from 145 formerly cryptorchid patients and 36 adult male controls. Single-strand conformational polymorphism analysis was used for the mutation detection studies. Two mutations, R49X and P69L, and several polymorphisms were identified. Both mutations were located in the connecting peptide region of the protein. The frequency of INSL3/RLF gene mutations as a cause of cryptorchidism is low, because only 2 of 145 (1.4%) formerly cryptorchid patients were found to have mutations.

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9

Tomboc, M. "Insulin-like 3/Relaxin-Like Factor Gene Mutations Are Associated with Cryptorchidism." Journal of Clinical Endocrinology & Metabolism 85, no. 11 (November 1, 2000): 4013–18. http://dx.doi.org/10.1210/jc.85.11.4013.

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10

Ivell, Richard, and Ross A. D. Bathgate. "Reproductive Biology of the Relaxin-Like Factor (RLF/INSL3)1." Biology of Reproduction 67, no. 3 (September 1, 2002): 699–705. http://dx.doi.org/10.1095/biolreprod.102.005199.

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11

Hombach-Klonisch, Sabine, Johannes Kauffold, Tanja Rautenberg, Klaus Steger, Frank Tetens, Bernd Fischer, and Thomas Klonisch. "Relaxin-like factor (RLF) mRNA expression in the fallow deer." Molecular and Cellular Endocrinology 159, no. 1-2 (January 2000): 147–58. http://dx.doi.org/10.1016/s0303-7207(99)00190-2.

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12

Negishi, Shinichi, Yong Li, Arvydas Usas, Freddie H. Fu, and Johnny Huard. "The Effect of Relaxin Treatment on Skeletal Muscle Injuries." American Journal of Sports Medicine 33, no. 12 (December 2005): 1816–24. http://dx.doi.org/10.1177/0363546505278701.

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Background Injured skeletal muscle can repair itself via spontaneous regeneration; however, the overproduction of extracellular matrix and excessive collagen deposition lead to fibrosis. Neutralization of the effect of transforming growth factor-β1, a key fibrotic cytokine, on myogenic cell differentiation after muscle injury can prevent fibrosis, enhance muscle regeneration, and thereby improve the functional recovery of injured muscle. Hypothesis The hormone relaxin, a member of the family of insulin-like growth factors, can act as an antifibrosis agent and improve the healing of injured muscle. Study Design Controlled laboratory study. Methods In vitro: Myoblasts (C2C12 cells) and myofibroblasts (transforming growth factor-β1-transfected myoblasts) were incubated with relaxin, and cell growth and differentiation were examined. Myogenic and fibrotic protein expression was determined by Western blot analysis. In vivo: Relaxin was injected intramuscularly at different time points after laceration injury. Skeletal muscle healing was evaluated via histologic, immunohistochemical, and physiologic tests. Results Relaxin treatment resulted in a dose-dependent decrease in myofibroblast proliferation, down-regulated expression of the fibrotic protein α-smooth muscle actin, and promoted the proliferation and differentiation of myoblasts in vitro. Relaxin therapy enhanced muscle regeneration, reduced fibrosis, and improved injured muscle strength in vivo. Conclusion Administration of relaxin can significantly improve skeletal muscle healing. Clinical Relevance These findings may facilitate the development of techniques to eliminate fibrosis, enhance muscle regeneration, and improve functional recovery after muscle injuries.

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13

McDonald, Glenn A., Pradip Sarkar, Helmut Rennke, Elaine Unemori, Raghu Kalluri, and Vikas P. Sukhatme. "Relaxin increases ubiquitin-dependent degradation of fibronectin in vitro and ameliorates renal fibrosis in vivo." American Journal of Physiology-Renal Physiology 285, no. 1 (July 2003): F59—F67. http://dx.doi.org/10.1152/ajprenal.00157.2002.

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Fibronectin, a large adhesive glycoprotein, is a prominent constituent of the extracellular matrix. Abnormalities in fibronectin homeostasis occur in numerous disease states, ranging from primary fibrosing conditions to neoplastic transformation. We demonstrate that fibronectin is a target protein substrate for ubiquitin-dependent degradation. Coimmunoprecipitation experiments and confocal microscopy demonstrated ubiquitin-fibronectin interaction. In an in vitro model of renal fibrosis, relaxin, an insulin-like growth factor, increased ubiquitin-dependent fibronectin degradation. Relaxin also was evaluated in an anti-glomerular basement membrane model of renal fibrosis. Animals treated with relaxin experienced renoprotection, manifested by decreased serum creatinine and proteinuria. Histological evaluation of kidney sections from animals treated with relaxin showed decreased glomerulosclerosis and interstitial fibrosis. We conclude that relaxin might be developed as a useful agent for the treatment of renal fibrosis.

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14

Feng, Shu, Natalia V. Bogatcheva, Aparna A. Kamat, Anne Truong, and Alexander I. Agoulnik. "Endocrine Effects of Relaxin Overexpression in Mice." Endocrinology 147, no. 1 (January 1, 2006): 407–14. http://dx.doi.org/10.1210/en.2005-0626.

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Relaxin is a small peptide hormone with a variety of biological functions. To investigate the systemic endocrine effects of relaxin, we produced mice with transgenic overexpression of the Rln1 gene, Tg(Rln1), driven by rat insulin 2 promoter. The expression of relaxin was detected in the pancreas of the transgenic animals. An analysis of the sera from the transgenic animals revealed at least 20-fold elevation of the level of bioactive relaxin. Transgenic animals had normal viability and fertility in both sexes. Transgenic overexpression of Rln1 did not rescue the undescended testis phenotype in Insl3-deficient males, suggesting that in vivo relaxin does not interact with the insulin-like 3 factor receptor, leucine-rich repeats-containing G protein-coupled receptor 8, Lgr8. Phenotypically, the excess of relaxin resulted in hypertrophic nipple development in virgin female mice. Deletion of the relaxin receptor, leucine-rich repeats-containing G protein-coupled receptor 7, Lgr7, in Tg(Rln1) animals abrogated the development of enlarged nipples in females, indicating that relaxin exerts its effect through Lgr7 alone. The levels of previously defined targets of relaxin signaling, such as matrix metalloproteinases 2 and 9, vascular endothelial growth factor, or nitric oxide, were similar in the sera of the transgenic and wild-type mice. However, the total plasma protein concentration in male Tg(Rln1) mice was lower than that in control animals. The livers of male Tg(Rln1) mice exhibited significantly higher hydroxyproline content, indicative of increased collagen deposition. Our results indicate that relaxin overexpression causes gender-specific changes in liver collagen metabolism.

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15

Büllesbach, Erika E., Fredric R. Boockfor, George Fullbright, and Christian Schwabe. "Cryptorchidism induced in normal rats by the relaxin-like factor inhibitor." REPRODUCTION 135, no. 3 (March 2008): 351–55. http://dx.doi.org/10.1530/rep-07-0330.

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Cryptorchidism is a serious problem, which affects 2–5% of the male population. Failure of the testes to descend into the scrotal region impairs germ cell development and is associated with a greater incidence of testicular cancer. The relaxin-like factor (RLF or insulin-like-3) has been shown to be critically important for the timely descent of the testicles in mice. We have discovered that the signal initiation site of the RLF can be eliminated without measurable effects on hormone binding to its receptor and that the resulting RLF derivative is a competitive inhibitor of RLF called RLFi. RLFi administered to pregnant rats causes dose-dependent gonadal retention in the offspring. The ability to control the severity of the syndrome by altering the concentration of RLFi and the timing of administration enables us to study in detail the structural changes that are associated with the action of RLF during critical stages of development. Targeted inhibition of the physiological migration pattern of testicles by RLFi lets one dissect the physiological process such as to find a window for clinical application of RLF and to search for ancillary factors that might play a role during normal development.

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16

Spiess, Andrej-Nikolai, Marga Balvers, Manuel Tena-Sempere, Ilpo Huhtaniemi, Laura Parry, and Richard Ivell. "Structure and expression of the rat relaxin-like factor (RLF) gene." Molecular Reproduction and Development 54, no. 4 (December 1999): 319–25. http://dx.doi.org/10.1002/(sici)1098-2795(199912)54:4<319::aid-mrd1>3.0.co;2-z.

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17

O'Sullivan, Kelly P., Sarah A. Marshall, Scott Cullen, Tahnee Saunders, Natalie J. Hannan, Sevvandi N. Senadheera, and Laura J. Parry. "Evidence of proteinuria, but no other characteristics of pre-eclampsia, in relaxin-deficient mice." Reproduction, Fertility and Development 29, no. 8 (2017): 1477. http://dx.doi.org/10.1071/rd16056.

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Pre-eclampsia (PE) is a leading cause of maternal and fetal death, characterised by an imbalance of placental growth factors and hypertension at >20 weeks gestation. Impaired maternal systemic vascular adaptations and fetal growth restriction are features of both PE and pregnant relaxin-deficient (Rln–/–) mice. The aim of the present study was to investigate whether these phenotypes in Rln–/– mice are associated with abnormal placental growth factor expression, increased soluble fms-like tyrosine kinase-1 (sFlt-1), proteinuria and/or hypertension during pregnancy. In addition, we examined relaxin and relaxin receptor (relaxin/insulin like family peptide receptor 1 (RXFP1)) mRNA expression in placentas of women with PE. There was no significant difference in placental vascular endothelial growth factor A (VegfA) and placenta growth factor (Plgf) gene expression between Rln–/– and wild-type mice. Circulating plasma sFlt-1 concentrations in pregnant mice of both genotypes and ages were increased compared with non-pregnant mice but were lower in younger pregnant Rln–/– mice compared with aged-matched Rln+/+ mice. Aged pregnant Rln–/– mice had higher urinary albumin : creatinine ratios compared with age-matched Rln+/+ mice, indicative of proteinuria. Systolic and diastolic blood pressures did not differ between genotypes. In addition, PE in women was not associated with altered placental mRNA expression of RLN2 or RXFP1 at term. Overall, the data demonstrate that pregnant Rln–/– mice do not have the typical characteristics of PE. However, these mice show evidence of proteinuria, but we suggest that this results from systemic renal vascular dysfunction before pregnancy.

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18

Merchav, Ronit, Yonatan Feuermann, Avi Shamay, Eyal Ranen, Uri Stein, Dudley E. Johnston, and Ron Shahar. "Expression of Relaxin Receptor LRG7, Canine Relaxin, and Relaxin-Like Factor in the Pelvic Diaphragm Musculature of Dogs with and Without Perineal Hernia." Veterinary Surgery 34, no. 5 (September 2005): 476–81. http://dx.doi.org/10.1111/j.1532-950x.2005.00072.x.

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19

NICHOLS, NICOLE, HILARY BINTA, PHILLIP A. FIELDS, MAARTEN DROST, SHOU-MEI CHANG, RICHARD IVELL, and MICHAEL J. FIELDS. "Immunohistochemical Localization of Relaxin-Like Factor/Insulin-Like Peptide-3 in the Bovine Corpus Luteum." Annals of the New York Academy of Sciences 1041, no. 1 (May 2005): 506–9. http://dx.doi.org/10.1196/annals.1282.075.

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20

Klonisch, Thomas, Sabine Hombach-Klonisch, Jörg Buchmann, Bernd Fischer, Martin Bergmann, and Klaus Steger. "Relaxin-like factor expression in a human ovarian Sertoli-Leydig cell tumor." Fertility and Sterility 72, no. 3 (September 1999): 546–48. http://dx.doi.org/10.1016/s0015-0282(99)00297-6.

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21

Kamat, Aparna A., Shu Feng, Natalia V. Bogatcheva, Anne Truong, Colin E. Bishop, and Alexander I. Agoulnik. "Genetic Targeting of Relaxin and Insulin-Like Factor 3 Receptors in Mice." Endocrinology 145, no. 10 (October 1, 2004): 4712–20. http://dx.doi.org/10.1210/en.2004-0515.

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Abstract Relaxin (RLN) is a small peptide hormone that affects a variety of biological processes. Rln1 knockout mice exhibit abnormal nipple development, prolonged parturition, agerelated pulmonary fibrosis, and abnormalities in the testes and prostate. We describe here RLN receptor Lgr7-deficient mice. Mutant females have grossly underdeveloped nipples and are unable to feed their progeny. Some Lgr7−/− females were unable to deliver their pups. Histological analysis of Lgr7 mutant lung tissues demonstrates increased collagen accumulation and fibrosis surrounding the bronchioles and the vascular bundles, absent in wild-type animals. However, Lgr7-deficient males do not exhibit abnormalities in the testes or prostate as seen in Rln1 knockout mice. Lgr7-deficient females with additional deletion of Lgr8 (Great), another putative receptor for RLN, are fertile and have normal-sized litters. Double mutant males have normal-sized prostate and testes, suggesting that Lgr8 does not account for differences in Rln1−/− and Lgr7−/− phenotypes. Transgenic overexpression of Insl3, the cognate ligand for Lgr8, does not rescue the mutant phenotype of Lgr7-deficient female mice indicating nonoverlapping functions of the two receptors. Our data indicate that neither Insl3 nor Lgr8 contribute to the RLN signaling pathway. We conclude that the Insl3/Lgr8 and Rln1/Lgr7 actions do not overlap in vivo.

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22

Büllesbach, Erika E., and Christian Schwabe. "A Novel Leydig Cell cDNA-derived Protein Is a Relaxin-like Factor." Journal of Biological Chemistry 270, no. 27 (July 7, 1995): 16011–15. http://dx.doi.org/10.1074/jbc.270.27.16011.

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23

Koskimies, Pasi, Jérôme Levallet, Petra Sipilä, Ilpo Huhtaniemi, and Matti Poutanen. "Murine Relaxin-Like Factor Promoter: Functional Characterization and Regulation by Transcription Factors Steroidogenic Factor 1 and DAX-1." Endocrinology 143, no. 3 (March 2002): 909–19. http://dx.doi.org/10.1210/endo.143.3.8683.

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24

Minagawa, Itaru, Dai Sagata, Ali Mohammed Pitia, Hiroshi Kohriki, Masatoshi Shibata, Hiroshi Sasada, Yoshihisa Hasegawa, and Tetsuya Kohsaka. "Dynamics of insulin-like factor 3 and its receptor expression in boar testes." Journal of Endocrinology 220, no. 3 (March 2014): 247–61. http://dx.doi.org/10.1530/joe-13-0430.

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Relaxin-like factor (RLF), now mainly known as insulin-like factor 3 (INSL3), is essential for testis descent during fetal development; however, its function in the adult testis is still being elucidated. As a major step toward understanding the as-yet-unknown function of INSL3 in boars, this study aimed to develop a time-resolved fluoroimmunoassay for boar INSL3, characterize the dynamics of INSL3 expression during development, and demonstrate the expression of the INSL3 hormone–receptor system in the testis. All samples were collected from Duroc boars. The sensitivity of the assay system established was 8.2 pg/well (164 pg/ml), and no cross-reactivity with other hormones, such as porcine relaxin, was observed. Circulating INSL3 was shown to increase progressively during development. INSL3 secreted from the Leydig cells was released not only into the blood circulation but also into the interstitial and seminiferous compartments in sufficient concentrations. A testicular fractionation study revealed that its receptor RXFP2 transcripts were expressed mainly in testicular germ cells. In addition, INSL3 bound to the germ cell membranes in a hormone-specific and saturable manner. These results reveal that INSL3 secreted into the interstitial compartment from the Leydig cells is transported into the seminiferous compartments, where its receptor RXFP2 is expressed mainly in the germ cells to which INSL3 binds, suggesting that INSL3 functions as a paracrine factor on seminiferous germ cells.

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25

Pusch, W., M. Balvers, and R. Ivell. "Molecular cloning and expression of the relaxin-like factor from the mouse testis." Endocrinology 137, no. 7 (July 1996): 3009–13. http://dx.doi.org/10.1210/endo.137.7.8770925.

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26

Hombach-Klonisch, S. "Cellular localization of human relaxin-like factor in the cyclic endometrium and placenta." Molecular Human Reproduction 7, no. 4 (April 1, 2001): 349–56. http://dx.doi.org/10.1093/molehr/7.4.349.

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27

Toth, M., P. Taskinen, and H. Ruskoaho. "Relaxin stimulates atrial natriuretic peptide secretion in perfused rat heart." Journal of Endocrinology 150, no. 3 (September 1996): 487–95. http://dx.doi.org/10.1677/joe.0.1500487.

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Abstract Relaxin, a reproductive hormone of the insulin-like growth factor family, increases heart rate in experimental animals but its other actions on cardiac function and cellular mechanisms responsible for the positive chronotrophic effect remain unknown. We have studied the actions of human recombinant gene-2 relaxin on the release of atrial natriuretic peptide (ANP) and cardiac function (heart rate, contractile force, perfusion pressure) as well as the underlying signal transduction mechanisms by using the isolated perfused spontaneously beating rat heart preparation. The administration of relaxin into the perfusion fluid at concentrations of 1·5, 3 or 10 nm for 30 min caused a dose-dependent sustained increase in heart rate, while contractile force and perfusion pressure remained unchanged. In addition, infusion of relaxin at a concentration of 10 nm into the perfusate produced a gradual 1·5-fold increase in immunoreactive ANP (IR-ANP) secretion (from 456 ± 76 to 701 ± 124 pg/ml, F=4·5, P<0·001). The ANP secretory and chronotrophic effects of relaxin appear to involve the activation of protein kinase C, since administration of a protein kinase C inhibitor staurosporine at a concentration of 30 nm completely blocked the effect of relaxin (10 nm) on IR-ANP secretion P<0·001) and heart rate (P<0·001). A cAMP-dependent protein kinase inhibitor, H-89 (100 nm), also substantially reduced the ANP secretory effect of relaxin and attenuated the increase in heart rate during the sustained phase of the relaxin infusion (P<0·001). KN-62 (3 μm), a Ca2+/calmodulin-dependent protein kinase inhibitor, decreased the positive chronotrophic effect of relaxin (P<0·001) but did not influence significantly the effect of relaxin on IR-ANP release in isolated perfused rat heart preparation. These results provide the first evidence that relaxin stimulates the secretion of ANP from isolated perfused rat hearts. Our results also suggest that relaxin modulates ANP secretion by activation of protein kinase C and cAMP-dependent protein kinase pathways. Journal of Endocrinology (1996) 150, 487–495

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28

Minagawa, Itaru, Masafumi Fukuda, Hisako Ishige, Hiroshi Kohriki, Masatoshi Shibata, Enoch Y. Park, Tatsuo Kawarasaki, and Tetsuya Kohsaka. "Relaxin-like factor (RLF)/insulin-like peptide 3 (INSL3) is secreted from testicular Leydig cells as a monomeric protein comprising three domains B–C–A with full biological activity in boars." Biochemical Journal 441, no. 1 (December 14, 2011): 265–73. http://dx.doi.org/10.1042/bj20111107.

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RLF (relaxin-like factor), also known as INSL3 (insulin-like peptide 3), is a novel member of the relaxin/insulin gene family that is expressed in testicular Leydig cells. Despite the implicated role of RLF/INSL3 in testis development, its native conformation remains unknown. In the present paper we demonstrate for the first time that boar testicular RLF/INSL3 is isolated as a monomeric structure with full biological activity. Using a series of chromatography steps, the native RLF/INSL3 was highly purified as a single peak in reverse-phase HPLC. MS/MS (tandem MS) analysis of the trypsinized sample provided 66% sequence coverage and revealed a distinct monomeric structure consisting of the B-, C- and A-domains deduced previously from the RLF/INSL3 cDNA. Moreover, the N-terminal peptide was four amino acid residues longer than predicted previously. MS analysis of the intact molecule and PMF (peptide mass fingerprinting) analysis at 100% sequence coverage confirmed this structure and indicated the existence of three site-specific disulfide bonds. RLF/INSL3 retained full bioactivity in HEK (human embryonic kidney)-293 cells expressing RXFP2 (relaxin/insulin-like family peptide receptor 2), the receptor for RLF/INSL3. Furthermore, RLF/INSL3 was found to be secreted from Leydig cells into testicular venous blood. Collectively, these results indicate that boar RLF/INSL3 is secreted from testicular Leydig cells as a B–C–A monomeric structure with full biological activity.

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29

van Drongelen, Joris, Ivo H. J. Ploemen, Jeanne Pertijs, Jonathan H. Gooi, Fred C. G. J. Sweep, Frederik K. Lotgering, Marc E. A. Spaanderman, and Paul Smits. "Aging attenuates the vasodilator response to relaxin." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (May 2011): H1609—H1615. http://dx.doi.org/10.1152/ajpheart.00360.2010.

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Relaxin, an insulin-like growth factor peptide, increases endothelium-dependent vasodilation and vascular compliance and decreases myogenic reactivity. These vascular effects significantly contribute to the physiological circulatory adaptations in pregnancy, particularly in the mesentery and kidney. Aging predisposes to vascular maladaptation and gestational hypertensive disease. We hypothesized that mild aging reduces the vascular responses to relaxin. In 20 young (10–12 wk) and 20 middle-aged (40–46 wk) female Wistar Hannover rats, vascular responses to chronic exposure of relaxin vs. placebo (5 days) were quantified in isolated mesenteric arteries and kidney. Vascular responses were evaluated using pressure-perfusion myograph, wire myograph, and an isolated perfused rat kidney model. Rxfp1 (relaxin family peptide) gene expression was determined by quantitative polymerase chain reaction. In young rats, relaxin stimulated nitric oxide (NO)-dependent flow-mediated vasodilation (2.67-fold, from 48 ± 9 to 18 ± 4 μl/min), reduced myogenic reactivity (from −1 ± 2 to 7 ± 3 μm/10 mmHg), and decreased mesenteric sensitivity to (28%, from 1.39 ± 0.08 to 1.78 ± 0.10 μM) but did not change compliance and renal perfusion flow (RPFF). In aged rats, relaxin did not affect any of the analyzed mesenteric or renal parameters. In aged compared with young placebo-treated rats, all mesenteric characteristics were comparable, while RPFF was lower (17%, from 6.9 ± 0.2 to 5.7 ± 0.1 ml·min−1·100 g−1) even though NO availability was comparable. Rxfp1 expression was not different among young and aged rats. Our findings suggest that moderate aging involves normal endothelial function but blunts the physiological endothelium-dependent and -independent vasodilator response to relaxin.

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30

Büllesbach, Erika E., and Christian Schwabe. "Tryptophan B27 in the Relaxin-like Factor (RLF) Is Crucial for RLF Receptor-Binding†." Biochemistry 38, no. 10 (March 1999): 3073–78. http://dx.doi.org/10.1021/bi982687u.

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31

Büllesbach, Erika E., and Christian Schwabe. "Structure of the Transmembrane Signal Initiation Site of the Relaxin-Like Factor (RLF/INSL3)†." Biochemistry 46, no. 34 (August 2007): 9722–27. http://dx.doi.org/10.1021/bi700708s.

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32

Büllesbach, Erika E., and Christian Schwabe. "The Primary Structure and the Disulfide Links of the Bovine Relaxin-like Factor (RLF)†." Biochemistry 41, no. 1 (January 2002): 274–81. http://dx.doi.org/10.1021/bi0117302.

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33

Klonisch, T. "Expression of relaxin-like factor is down-regulated in human testicular Leydig cell neoplasia." Molecular Human Reproduction 5, no. 2 (February 1, 1999): 104–8. http://dx.doi.org/10.1093/molehr/5.2.104.

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34

Büllesbach, Erika E., Mathias A. S. Hass, Malene R. Jensen, D. Flemming Hansen, Søren M. Kristensen, Christian Schwabe, and Jens J. Led. "Solution Structure of a Conformationally Restricted Fully Active Derivative of the Human Relaxin-like Factor†‡." Biochemistry 47, no. 50 (December 16, 2008): 13308–17. http://dx.doi.org/10.1021/bi801412w.

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35

Koskimies, Pasi, Helena Virtanen, Magdalena Lindström, Marko Kaleva, Matti Poutanen, Ilpo Huhtaniemi, and Jorma Toppari. "A Common Polymorphism in the Human Relaxin-Like Factor (RLF) Gene: No Relationship with Cryptorchidism." Pediatric Research 47, no. 4 (April 2000): 538–41. http://dx.doi.org/10.1203/00006450-200004000-00020.

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36

Millar, Lynnae K., Roxanne Reiny, Sandra Y. Yamamoto, Kristie Okazaki, Lisa Webster, and Gillian D. Bryant-Greenwood. "Relaxin causes proliferation of human amniotic epithelium by stimulation of insulin-like growth factor-II." American Journal of Obstetrics and Gynecology 188, no. 1 (January 2003): 234–41. http://dx.doi.org/10.1067/mob.2003.80.

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Balvers, M., A. N. Spiess, R. Domagalski, N. Hunt, E. Kilic, A. K. Mukhopadhyay, E. Hanks, H. M. Charlton, and R. Ivell. "Relaxin-Like Factor Expression as a Marker of Differentiation in the Mouse Testis and Ovary1." Endocrinology 139, no. 6 (June 1998): 2960–70. http://dx.doi.org/10.1210/endo.139.6.6046.

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Hombach-Klonisch, Sabine, Joerg Buchmann, Sukhena Sarun, Bernd Fischer, and Thomas Klonisch. "Relaxin-like factor (RLF) is differentially expressed in the normal and neoplastic human mammary gland." Cancer 89, no. 11 (2000): 2161–68. http://dx.doi.org/10.1002/1097-0142(20001201)89:11<2161::aid-cncr3>3.0.co;2-k.

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Hombach-Klonisch, Sabine, Frank Tetens, Johannes Kauffold, Klaus Steger, Bernd Fischer, and Thomas Klonisch. "Molecular cloning and localization of caprine relaxin-like factor (RLF) mRNA within the goat testis." Molecular Reproduction and Development 53, no. 2 (June 1999): 135–41. http://dx.doi.org/10.1002/(sici)1098-2795(199906)53:2<135::aid-mrd2>3.0.co;2-j.

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Ali, Samia, Zabun Nahar, Md Rajibur Rahman, Sardar Mohammad Ashraful Islam, Mohiuddin Ahmed Bhuiyan, and Md Rabiul Islam. "Serum insulin-like growth factor-1 and relaxin-3 are linked with major depressive disorder." Asian Journal of Psychiatry 53 (October 2020): 102164. http://dx.doi.org/10.1016/j.ajp.2020.102164.

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Klonisch, Thomas, Johannes Kauffold, Klaus Steger, Martin Bergmann, Rudolf Leiser, Bernd Fischer, and Sabine Hombach-Klonisch. "Canine Relaxin-Like Factor: Unique Molecular Structure and Differential Expression Within Reproductive Tissues of the Dog." Biology of Reproduction 64, no. 2 (February 1, 2001): 442–50. http://dx.doi.org/10.1095/biolreprod64.2.442.

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SIQIN, Mai KOTANI, Takuya AOSHIMA, Mari NAKAI, Mai FUCHIGAMI, Yuki ODANAKA, Yasushi SUGAWARA, et al. "Protein localization of relaxin-like factor in goat testes and its expression pattern during sexual development." Nihon Chikusan Gakkaiho 81, no. 1 (2010): 1–9. http://dx.doi.org/10.2508/chikusan.81.1.

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Lucas, C., L. N. Bald, M. C. Martin, R. B. Jaffe, D. W. Drolet, M. Mora-Worms, G. Bennett, A. B. Chen, and P. D. Johnston. "An enzyme-linked immunosorbent assay to study human relaxin in human pregnancy and in pregnant rhesus monkeys." Journal of Endocrinology 120, no. 3 (March 1989): 449–57. http://dx.doi.org/10.1677/joe.0.1200449.

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ABSTRACT A sensitive and specific double-antibody enzyme-linked immunoassay, using a synthetic analogue of human relaxin for standard and immunogen, was developed for the measurement of human relaxin (hRLX) in serum and plasma. No cross-reactivity was observed for human insulin, human insulin-like growth factor-I, hGH, human chorionic gonadotropin, hFSH, hLH or human prolactin. The assay was used to monitor RLX concentrations in samples from men, non-pregnant and pregnant women, and in pregnant rhesus monkeys infused with hRLX. RLX was not detected in serum from men nor from non-pregnant women, while a concentration of 600 ng/l was measured in pooled sera from two pregnant women (pregnancies achieved by in-vitro fertilization). Immunoreactive RLX (1·1 μg/g) was found in human corpora lutea taken from ectopic pregnancies at 7 weeks. In an experiment with a pregnant rhesus monkey infused with human RLX analogue, less than 1·5% of the maternal concentration was measured in the fetal circulation. Even though preliminary, these data suggest a low level of transfer of human analogue relaxin across the placenta in a rhesus monkey. Further studies of the physiology of RLX in human pregnancy will be facilitated by the availability of this immunoassay. Journal of Endocrinology (1989) 120, 449–457

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Ohleth, Kathleen M., and Carol A. Bagnell. "Relaxin-Induced Deoxyribonucleic Acid Synthesis in Porcine Granulosa Cells is Mediated by Insulin-Like Growth Factor-I1." Biology of Reproduction 53, no. 6 (December 1, 1995): 1286–92. http://dx.doi.org/10.1095/biolreprod53.6.1286.

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Tan, Yean Yeow, Nicola F. Dawson, Andrew R. Kompa, Courtney P. Bond, Antonia Claasz, John D. Wade, Geoffrey W. Tregear, and Roger J. Summers. "Structural requirements for the interaction of sheep insulin-like factor 3 with relaxin receptors in rat atria." European Journal of Pharmacology 457, no. 2-3 (December 2002): 153–60. http://dx.doi.org/10.1016/s0014-2999(02)02662-6.

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Büllesbach, Erika E., and Christian Schwabe. "Synthetic Cross-Links Arrest the C-Terminal Region of the Relaxin-like Factor in an Active Conformation†." Biochemistry 43, no. 25 (June 2004): 8021–28. http://dx.doi.org/10.1021/bi049601j.

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Ivell, R. "Relaxin-like factor: a highly specific and constitutive new marker for Leydig cells in the human testis." Molecular Human Reproduction 3, no. 6 (June 1, 1997): 459–66. http://dx.doi.org/10.1093/molehr/3.6.459.

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Xue, Kai, Ji Young Kim, Jia-yin Liu, and Benjamin K. Tsang. "Insulin-like 3-Induced Rat Preantral Follicular Growth Is Mediated by Growth Differentiation Factor 9." Endocrinology 155, no. 1 (January 1, 2014): 156–67. http://dx.doi.org/10.1210/en.2013-1491.

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The communication of somatic cells and oocytes by intrafollicular paracrine factors is essential for follicular growth in the ovary. Insulin-like 3 (INSL3) is a theca cell-secreted paracrine factor. Androgens and growth differentiation factor 9 (GDF9), an oocyte-derived growth factor, are essential for follicular development. Using a rat preantral follicle culture model, we examined in the present study the influence of INSL3 on preantral follicular growth and the molecular mechanisms involved. We have observed that the receptor for INSL3, relaxin/insulin-like family peptide receptor 2 (RXFP2), was exclusively expressed in oocytes. Recombinant INSL3 stimulated Gdf9 expression, preantral follicular growth, and testosterone synthesis in vitro. Inhibition of the cAMP/protein kinase A signaling pathway (with cAMP antagonist, 8-bromoadenosine 3′,5′-cyclic monophosphorothioate, Rp-isomer) attenuated INSL3-induced Gdf9 expression and preantral follicular growth. Moreover, knocking down Gdf9 expression (with small interfering RNA) or inhibiting GDF9 signaling (with SB431542, an activin receptor-like kinase receptor 5 inhibitor, or specific inhibitor of mothers against decapentaplegic homolog 3) or androgen action (with flutamide, an androgen receptor antagonist) suppressed INSL3-induced preantral follicular growth. In addition, LH and DHT regulated the expression of Insl3 mRNA in preantral follicles. These observations suggest that INSL3 is a key theca cell-derived growth factor for preantral follicle and that its action is mediated by GDF9.

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Siqin, Itaru Minagawa, Mitsutoshi Okuno, Kimihiko Yamada, Yasushi Sugawara, Yoshio Nagura, Koh-Ichi Hamano, Enoch Y. Park, Hiroshi Sasada, and Tetsuya Kohsaka. "The active form of goat insulin-like peptide 3 (INSL3) is a single-chain structure comprising three domains B-C-A, constitutively expressed and secreted by testicular Leydig cells." Biological Chemistry 394, no. 9 (September 1, 2013): 1181–94. http://dx.doi.org/10.1515/hsz-2012-0357.

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Abstract Relaxin-like factor (RLF), also called insulin-like peptide 3 (INSL3), is a member of the insulin/relaxin gene family and is produced by testicular Leydig cells. While the understanding of its effects is growing, very little is known about the structural and functional properties of native INSL3. Here, we demonstrate that native INSL3 isolated from goat testes is a single-chain structure with full biological activity, and is constitutively expressed and secreted by Leydig cells. Using a series of chromatography steps, native INSL3 was highly purified as a single 12-kDa peak as revealed by SDS-PAGE. MS/MS analysis provided 81% sequence coverage and revealed a distinct single-chain structure consisting of the B-, C-, and A-domains deduced previously from the INSL3 cDNA sequence. Moreover, the N-terminal peptide was six amino acid residues longer than predicted. Native INSL3 exhibited full bioactivity in HEK-293 cells expressing the receptor for INSL3. Immunoelectron microscopy and Western blot analysis revealed that INSL3 was secreted by Leydig cells through the constitutive pathway into blood and body fluids. We conclude, therefore, that goat INSL3 is constitutively secreted from Leydig cells as a B-C-A single-chain structure with full biological activity.

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Veenstra, Jan A. "Arthropod IGF, relaxin and gonadulin, putative orthologs of Drosophila insulin-like peptides 6, 7 and 8, likely originated from an ancient gene triplication." PeerJ 8 (July 10, 2020): e9534. http://dx.doi.org/10.7717/peerj.9534.

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Background Insects have several genes coding for insulin-like peptides and they have been particularly well studied in Drosophila. Some of these hormones function as growth hormones and are produced by the fat body and the brain. These act through a typical insulin receptor tyrosine kinase. Two other Drosophila insulin-like hormones are either known or suspected to act through a G-protein coupled receptor. Although insulin-related peptides are known from other insect species, Drosophila insulin-like peptide 8, one that uses a G-protein coupled receptor, has so far only been identified from Drosophila and other flies. However, its receptor is widespread within arthropods and hence it should have orthologs. Such putative orthologs were recently identified in decapods and have been called gonadulins. Methodology In an effort to identify gonadulins in other arthropods public genome assemblies and short-read archives from insects and other arthropods were explored for the presence of genes and transcripts coding insulin-like peptides and their putative receptors. Results Gonadulins were detected in a number of arthropods. In those species for which transcriptome data from the gonads is available insect gonadulin genes are expressed in the ovaries and at least in some species also in the testes. In some insects differences in gonadulin expression in the ovary between actively reproducing and non-reproducing females differs more than 100-fold. Putative orthologs of Drosophila ilp 6 were also identified. In several non-Dipteran insects these peptides have C-terminally extensions that are alternatively spliced. The predicted peptides have been called arthropod insulin-like growth factors. In cockroaches, termites and stick insects genes coding for the arthropod insulin-like growth factors, gonadulin and relaxin, a third insulin-like peptide, are encoded by genes that are next to one another suggesting that they are the result of a local gene triplication. Such a close chromosomal association was also found for the arthropod insulin-like growth factor and gonadulin genes in spiders. Phylogenetic tree analysis of the typical insulin receptor tyrosine kinases from insects, decapods and chelicerates shows that the insulin signaling pathway evolved differently in these three groups. The G-protein coupled receptors that are related to the Drosophila ilp 8 receptor similarly show significant differences between those groups. Conclusion A local gene triplication in an early ancestor likely yielded three genes coding gonadulin, arthropod insulin-like growth factor and relaxin. Orthologs of these genes are now commonly present in arthropods and almost certainly include the Drosophila insulin-like peptides 6, 7 and 8.

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