Navigating the Shallows and Rapids of Cholesterol Synthesis Downstream of HMGCR

Sharpe, Laura J.; Howe, Vicky; Prabhu, Anika V.; Luu, Winnie; Brown, Andrew

doi:10.3177/jnsv.61.s154

Cited by 4 publications

(1 citation statement)

References 22 publications

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“…It has been reported that cholesterol biosynthesis and transformation play an important role in keeping the homeostasis of cholesterol in hepatocytes ( Li et al, 2021 ). The 3-hydroxy-3-methylglutaryl-CoA reductase ( HMGCR ) is the rate-limiting enzyme involved in the biosynthesis of cholesterol ( Sharpe et al, 2015 ). And cholesterol 7α hydroxylase ( CYP7A1 ) is involved in the first step in the transformation of cholesterol to bile acids in liver ( Wang et al, 1998 ).…”

Section: Introductionmentioning

confidence: 99%

Betaine supplementation alleviates corticosterone-induced hepatic cholesterol accumulation through epigenetic modulation of HMGCR and CYP7A1 genes in laying hens

Wu,

Zhang,

Meng

et al. 2024

Poultry Science

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Section: Introductionmentioning

confidence: 99%

Betaine supplementation alleviates corticosterone-induced hepatic cholesterol accumulation through epigenetic modulation of HMGCR and CYP7A1 genes in laying hens

Wu,

Zhang,

Meng

et al. 2024

Poultry Science

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Human cytomegalovirus infection impairs neural differentiation via repressing sterol regulatory element binding protein 2-mediated cholesterol biosynthesis

Li,

Sun,

et al. 2024

Cell. Mol. Life Sci.

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Congenital human cytomegalovirus (HCMV) infection is a major cause of abnormalities and disorders in the central nervous system (CNS) and/or the peripheral nervous system (PNS). However, the complete pathogenesis of neural differentiation disorders caused by HCMV infection remains to be fully elucidated. Stem cells from human exfoliated deciduous teeth (SHEDs) are mesenchymal stem cells (MSCs) with a high proliferation and neurogenic differentiation capacity. Since SHEDs originate from the neural crest of the early embryonic ectoderm, SHEDs were hypothesized to serve as a promising cell line for investigating the pathogenesis of neural differentiation disorders in the PNS caused by congenital HCMV infection. In this work, SHEDs were demonstrated to be fully permissive to HCMV infection and the virus was able to complete its life cycle in SHEDs. Under neurogenic inductive conditions, HCMV infection of SHEDs caused an abnormal neural morphology. The expression of stem/neural cell markers was also disturbed by HCMV infection. The impairment of neural differentiation was mainly due to a reduction of intracellular cholesterol levels caused by HCMV infection. Sterol regulatory element binding protein-2 (SREBP2) is a critical transcription regulator that guides cholesterol synthesis. HCMV infection was shown to hinder the migration of SREBP2 into nucleus and resulted in perinuclear aggregations of SREBP2 during neural differentiation. Our findings provide new insights into the prevention and treatment of nervous system diseases caused by congenital HCMV infection.

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