Identification of protease serine S1 family member 53 as a mitochondrial protein in murine islet beta cells
Autor: | Katsuhiko Yoshimoto, Noriko Mizusawa, Mitsuo Itakura, Takeo Iwata, Nagakatsu Harada, Izumi Ohigashi |
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Rok vydání: | 2021 |
Předmět: |
Signal peptide
Endocrinology Diabetes and Metabolism medicine.medical_treatment Immunoelectron microscopy Mitochondrion Mitochondrial Proteins Serine Islets of Langerhans Mice Endocrinology Downregulation and upregulation Insulin-Secreting Cells medicine Animals Insulin pancreatic β-cell Expressed sequence tag Gene knockdown Protease Chemistry Molecular biology mitochondria Glucose MIN6 Serine Proteases Prss53 Research Article |
Zdroj: | Islets article-version (VoR) Version of Record |
ISSN: | 1938-2022 1938-2014 |
Popis: | 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. |
Databáze: | OpenAIRE |
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