Beta-cell β1 Integrin Deficiency During Second Transition Stage Of Fetal Pancreas Development On Islet Growth
Abstract
β1 integrin has been shown to be important for pancreatic beta-cell growth and functioning. Congenital and postnatal studies have shown beta-cell mass reduction with β1 integrin knockout (β1KO). Using an inducible cre recombinase (CreERT) expressed from the mouse insulin promoter (MIP) crossed to a line in which Itgb1 (β1 integrin encoding gene) was flanked by loxP sites (MIP-CreERT+; β1itg designated as MIPβ1KO), we examined the in vivo temporal role of beta-cell β1 integrin effect on islet growth during the second transition stage of pancreas development.
Prenatal MIPβ1KO mice displayed decreased beta-cell area, mass, density and proliferation. In addition, a decrease in phosphorylated-ERK activity, islet vascularization and nascent endocrine cells in the ductal region was observed. However, normal levels of transcription factors needed for beta-cell development was seen. This study may suggest that β1 integrin plays an important role in prenatal beta-cell development during the second transition stage.