Identification of protease serine S1 family member 53 as a mitochondrial protein in murine islet beta cells. Issue 1 (1st January 2022)

• Record Type: Journal Article
• Authors: Mizusawa, Noriko; Harada, Nagakatsu; Iwata, Takeo; Ohigashi, Izumi; Itakura, Mitsuo; Yoshimoto, Katsuhiko
• Is Part Of: Islets. Volume 14:Issue 1(2022)
• Page Start: 1
• Page End: 13
• Publication Date: 2022-01-01
• Subjects: Prss53 -- pancreatic β-cell -- MIN6 -- mitochondria; Islands of Langerhans -- Periodicals; Pancreas -- Periodicals; 616.46
• DOI: 10.1080/19382014.2021.1982325
• Languages: English
• ISSNs: 1938-2022

Abstract

ABSTRACT: The aim of this study was to identify genes that are specifically expressed in pancreatic islet β-cells (hereafter referred to as β-cells). Large-scale complementary DNA-sequencing analysis was performed for 3, 429 expressed sequence tags derived from murine MIN6 β-cells, through homology comparisons using the GenBank database. Three individual ESTs were found to code for protease serine S1 family member 53 ( Prss53 ). Prss53 mRNA is processed into both a short and long form, which encode 482 and 552 amino acids, respectively. Transient overexpression of myc-tagged Prss53 in COS-7 cells showed that Prss53 was strongly associated with the luminal surfaces of organellar membranes and that it underwent signal peptide cleavage and N-glycosylation. Immunoelectron microscopy and western blotting revealed that Prss53 localized to mitochondria in MIN6 cells. Short hairpin RNA-mediated Prss53 knockdown resulted in Ppargc1a downregulation and Ucp2 and Glut2 upregulation. JC-1 staining revealed that the mitochondria were depolarized in Prss53 -knockdown MIN6 cells; however, no change was observed in glucose-stimulated insulin secretion. Our results suggest that mitochondrial Prss53 expression plays an important role in maintaining the health of β-cells.