Loss of SNORA73 reprograms cellular metabolism and protects against steatohepatitis

Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are...

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Published inNature communications Vol. 12; no. 1; pp. 5214 - 17
Main Authors Sletten, Arthur C., Davidson, Jessica W., Yagabasan, Busra, Moores, Samantha, Schwaiger-Haber, Michaela, Fujiwara, Hideji, Gale, Sarah, Jiang, Xuntian, Sidhu, Rohini, Gelman, Susan J., Zhao, Shuang, Patti, Gary J., Ory, Daniel S., Schaffer, Jean E.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.09.2021
Nature Publishing Group
Nature Portfolio
Subjects
13
13/31
13/89
38
38/91
631/337/384/521
631/45/287
692/699/317
96
Animals
Apoptosis
Cell death
Cell Death - drug effects
CHO Cells
Cricetulus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Dyslipidemia
Fatty liver
Fatty Liver - drug therapy
Fatty Liver - genetics
Fatty Liver - metabolism
Homeostasis
Humanities and Social Sciences
Inflammation
Lipid Metabolism
Lipids
Lipids - pharmacology
Male
Metabolic disorders
Metabolic syndrome
Metabolic Syndrome - metabolism
Metabolism
Mice
Mice, Inbred C57BL
multidisciplinary
Nucleoli
Oxidation resistance
Oxidative metabolism
Oxidative stress
Oxidative Stress - drug effects
Protective Agents - pharmacology
Rapamycin
Ribonucleic acid
RNA
RNA, Long Noncoding
RNA, Small Nucleolar - genetics
RNA, Small Nucleolar - metabolism
Science
Science (multidisciplinary)
Signal Transduction - drug effects
snoRNA
Steatosis
TOR protein
Online AccessGet full text

Cover

Abstract Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3 ) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity. Lipid induced stress contributes to metabolic diseases. Here the authors identify small nucleolar RNA 73 (SNORA73) in a screen for genes that protect against lipotoxicity and show that deficiency of SNORA73 reprograms oxidative metabolism and protects against steatohepatitis in mice.
AbstractList Lipid induced stress contributes to metabolic diseases. Here the authors identify small nucleolar RNA 73 (SNORA73) in a screen for genes that protect against lipotoxicity and show that deficiency of SNORA73 reprograms oxidative metabolism and protects against steatohepatitis in mice.
Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity.Lipid induced stress contributes to metabolic diseases. Here the authors identify small nucleolar RNA 73 (SNORA73) in a screen for genes that protect against lipotoxicity and show that deficiency of SNORA73 reprograms oxidative metabolism and protects against steatohepatitis in mice.
Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3 ) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity.
Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity.Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity.
Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3 ) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity. Lipid induced stress contributes to metabolic diseases. Here the authors identify small nucleolar RNA 73 (SNORA73) in a screen for genes that protect against lipotoxicity and show that deficiency of SNORA73 reprograms oxidative metabolism and protects against steatohepatitis in mice.
Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces cell death through pleiotropic mechanisms that link to oxidative stress. However, pathways that regulate the response to metabolic stress are not well understood. Herein, we show that disruption of the box H/ACA SNORA73 small nucleolar RNAs encoded within the small nucleolar RNA hosting gene 3 (Snhg3) causes resistance to lipid-induced cell death and general oxidative stress in cultured cells. This protection from metabolic stress is associated with broad reprogramming of oxidative metabolism that is dependent on the mammalian target of rapamycin signaling axis. Furthermore, we show that knockdown of SNORA73 in vivo protects against hepatic steatosis and lipid-induced oxidative stress and inflammation. Our findings demonstrate a role for SNORA73 in the regulation of metabolism and lipotoxicity.
ArticleNumber 5214
Author Zhao, Shuang
Gelman, Susan J.
Moores, Samantha
Sletten, Arthur C.
Gale, Sarah
Sidhu, Rohini
Ory, Daniel S.
Yagabasan, Busra
Patti, Gary J.
Davidson, Jessica W.
Schwaiger-Haber, Michaela
Fujiwara, Hideji
Jiang, Xuntian
Schaffer, Jean E.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34471131$$D View this record in MEDLINE/PubMed
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Snippet Dyslipidemia and resulting lipotoxicity are pathologic signatures of metabolic syndrome and type 2 diabetes. Excess lipid causes cell dysfunction and induces...
Lipid induced stress contributes to metabolic diseases. Here the authors identify small nucleolar RNA 73 (SNORA73) in a screen for genes that protect against...
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StartPage 5214
SubjectTerms 13
13/31
13/89
38
38/91
631/337/384/521
631/45/287
692/699/317
96
Animals
Apoptosis
Cell death
Cell Death - drug effects
CHO Cells
Cricetulus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Dyslipidemia
Fatty liver
Fatty Liver - drug therapy
Fatty Liver - genetics
Fatty Liver - metabolism
Homeostasis
Humanities and Social Sciences
Inflammation
Lipid Metabolism
Lipids
Lipids - pharmacology
Male
Metabolic disorders
Metabolic syndrome
Metabolic Syndrome - metabolism
Metabolism
Mice
Mice, Inbred C57BL
multidisciplinary
Nucleoli
Oxidation resistance
Oxidative metabolism
Oxidative stress
Oxidative Stress - drug effects
Protective Agents - pharmacology
Rapamycin
Ribonucleic acid
RNA
RNA, Long Noncoding
RNA, Small Nucleolar - genetics
RNA, Small Nucleolar - metabolism
Science
Science (multidisciplinary)
Signal Transduction - drug effects
snoRNA
Steatosis
TOR protein
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Title Loss of SNORA73 reprograms cellular metabolism and protects against steatohepatitis
URI https://link.springer.com/article/10.1038/s41467-021-25457-y
https://www.ncbi.nlm.nih.gov/pubmed/34471131
https://www.proquest.com/docview/2568102825
https://www.proquest.com/docview/2568597154
https://pubmed.ncbi.nlm.nih.gov/PMC8410784
https://doaj.org/article/d0b59c5a040d41be8c7d87c9047d2474
Volume 12
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