| First Author | Win PW | Year | 2020 |
| Journal | Cell Tissue Res | Volume | 381 |
| Issue | 1 | Pages | 163-175 |
| PubMed ID | 32060653 | Mgi Jnum | J:309386 |
| Mgi Id | MGI:6754748 | Doi | 10.1007/s00441-020-03179-9 |
| Citation | Win PW, et al. (2020) Beta-cell beta1 integrin deficiency affects in utero development of islet growth and vascularization. Cell Tissue Res 381(1):163-175 |
| abstractText | The beta1 integrin subunit contributes to pancreatic beta cell growth and function through communication with the extracellular matrix (ECM). The effects of in vitro and in vivo beta1 integrin knockout have been extensively studied in mature islets, yet no study to date has examined how the loss of beta1 integrin during specific stages of pancreatic development impacts beta cell maturation. Beta-cell-specific tamoxifen-inducible Cre recombinase (MIP-CreERT) mice were crossed with mice containing floxed Itgb1 (beta1 integrin) to create an inducible mouse model (MIPbeta1KO) at the second transition stage (e13.5) of pancreas development. By e19.5-20.5, the expression of beta-cell beta1 integrin in fetal MIPbeta1KO mice was significantly reduced and these mice displayed decreased beta cell mass, density and proliferation. Morphologically, fetal MIPbeta1KO pancreata exhibited reduced islet vascularization and nascent endocrine cells in the ductal region. In addition, decreased ERK phosphorylation was observed in fetal MIPbeta1KO pancreata. The expression of transcription factors needed for beta-cell development was unchanged in fetal MIPbeta1KO pancreata. The findings from this study demonstrate that beta1 integrin signaling is required during a transition-specific window in the developing beta-cell to maintain islet mass and vascularization. |
