PMID- 35318102
OWN - NLM
STAT- MEDLINE
DCOM- 20220406
LR  - 20220708
IS  - 1873-4596 (Electronic)
IS  - 0891-5849 (Linking)
VI  - 183
DP  - 2022 Apr
TI  - Role of selenoprotein P expression in the function of pancreatic beta cells: 
      Prevention of ferroptosis-like cell death and stress-induced nascent granule 
      degradation.
PG  - 89-103
LID - S0891-5849(22)00104-6 [pii]
LID - 10.1016/j.freeradbiomed.2022.03.009 [doi]
AB  - Selenoprotein P (SELENOP) is a major selenium (Se)-containing protein 
      (selenoprotein) in human plasma that is mainly synthesized in the liver. SELENOP 
      transports Se to the cells, while SELENOP synthesized in peripheral tissues is 
      incorporated in a paracrine/autocrine manner to maintain the levels of cellular 
      selenoproteins, called the SELENOP cycle. Pancreatic beta cells, responsible for the 
      synthesis and secretion of insulin, are known to express SELENOP. Here, using 
      MIN6 cells as a mouse model for pancreatic beta cells and Selenop small interfering 
      (si)RNA, we found that Selenop gene knockdown (KD) resulted in decreased cell 
      viability, cellular pro/insulin levels, insulin secretion, and levels of several 
      cellular selenoproteins, including glutathione peroxidase 4 (Gpx4) and 
      selenoprotein K (Selenok). These dysfunctions induced by Selenop siRNA were 
      recovered by the addition of Se. Ferroptosis-like cell death, regulated by Gpx4, 
      was involved in the decrease of cell viability by Selenop KD, while 
      stress-induced nascent granule degradation (SINGD), regulated by Selenok, was 
      responsible for the decrease in proinsulin. SINGD was also observed in the 
      pancreatic beta cells of Selenop knockout mice. These findings indicate a 
      significant role of SELENOP expression for the function of pancreatic beta cells by 
      maintaining the levels of cellular selenoproteins such as GPX4 and SELENOK.
CI  - Copyright (c) 2022 Elsevier Inc. All rights reserved.
FAU - Kitabayashi, Nanako
AU  - Kitabayashi N
AD  - The Systems Life Sciences Laboratory, Department of Medical Life Systems, Faculty 
      of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
FAU - Nakao, Shohei
AU  - Nakao S
AD  - The Systems Life Sciences Laboratory, Department of Medical Life Systems, Faculty 
      of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
FAU - Mita, Yuichiro
AU  - Mita Y
AD  - The Systems Life Sciences Laboratory, Department of Medical Life Systems, Faculty 
      of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
FAU - Arisawa, Kotoko
AU  - Arisawa K
AD  - Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical 
      Sciences, Tohoku University, Sendai, 980-8578, Japan.
FAU - Hoshi, Takayuki
AU  - Hoshi T
AD  - Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical 
      Sciences, Tohoku University, Sendai, 980-8578, Japan.
FAU - Toyama, Takashi
AU  - Toyama T
AD  - Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical 
      Sciences, Tohoku University, Sendai, 980-8578, Japan.
FAU - Ishii, Kiyo-Aki
AU  - Ishii KA
AD  - Department of Endocrinology and Metabolism, Kanazawa University Graduate School 
      of Medical Sciences, Kanazawa, 920-8640, Japan.
FAU - Takamura, Toshinari
AU  - Takamura T
AD  - Department of Endocrinology and Metabolism, Kanazawa University Graduate School 
      of Medical Sciences, Kanazawa, 920-8640, Japan.
FAU - Noguchi, Noriko
AU  - Noguchi N
AD  - The Systems Life Sciences Laboratory, Department of Medical Life Systems, Faculty 
      of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
FAU - Saito, Yoshiro
AU  - Saito Y
AD  - The Systems Life Sciences Laboratory, Department of Medical Life Systems, Faculty 
      of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan; 
      Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical 
      Sciences, Tohoku University, Sendai, 980-8578, Japan. Electronic address: 
      yoshiro.saito.a8@tohoku.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20220319
PL  - United States
TA  - Free Radic Biol Med
JT  - Free radical biology & medicine
JID - 8709159
RN  - 0 (Selenop protein, mouse)
RN  - 0 (Selenoprotein P)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - H6241UJ22B (Selenium)
SB  - IM
MH  - Animals
MH  - *Ferroptosis
MH  - Glutathione Peroxidase/genetics/metabolism
MH  - *Insulin-Secreting Cells/metabolism
MH  - Mice
MH  - *Selenium/metabolism
MH  - *Selenoprotein P/genetics/metabolism
OTO - NOTNLM
OT  - Ferroptosis
OT  - GPX4
OT  - Pancreatic beta cells
OT  - Selenoprotein K
OT  - Selenoprotein P
OT  - Stress-induced nascent granule degradation (SINGD)
EDAT- 2022/03/24 06:00
MHDA- 2022/04/07 06:00
CRDT- 2022/03/23 05:37
PHST- 2022/02/02 00:00 [received]
PHST- 2022/03/07 00:00 [revised]
PHST- 2022/03/11 00:00 [accepted]
PHST- 2022/03/24 06:00 [pubmed]
PHST- 2022/04/07 06:00 [medline]
PHST- 2022/03/23 05:37 [entrez]
AID - S0891-5849(22)00104-6 [pii]
AID - 10.1016/j.freeradbiomed.2022.03.009 [doi]
PST - ppublish
SO  - Free Radic Biol Med. 2022 Apr;183:89-103. doi: 
      10.1016/j.freeradbiomed.2022.03.009. Epub 2022 Mar 19.