Roles of Histone Acetyltransferases and Deacetylases in the Retinal Development and Diseases

Wang, Jingjing; Feng, Shuyu; Zhang, Qian; Qin, Huan; Xu, Chunxiu; Fu, Xuefei; Lin, Yan; Zhao, Yaqin; Yao, Kai

doi:10.1007/s12035-023-03213-1

Cited by 5 publications

(5 citation statements)

References 194 publications

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“…Histone acetylation modifications are important epigenetics regulated by histone acetyltransferases (HATs) and HDACs 32 , 33 . To investigate whether HDACs are involved in the heat shock-induced decrease of H3K9ac, we screened major classes of HDAC inhibitors.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of Heat Shock-Induced H3K9ac Reduction Sensitizes Cancer Cells to Hyperthermia

Lin,

Song,

Song

et al. 2023

Int. J. Biol. Sci.

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Heat stress, clinically known as hyperthermia, is a promising adjunctive modality in cancer treatment. However, the efficacy of hyperthermia as a monotherapy is limited and the underlying mechanism remains poorly understood. Targeting histone modifications is an emerging strategy for cancer therapy, but little is known regarding the role of heat stress in altering these modifications. Here, we report that heat shock inhibits H3K9 acetylation (H3K9ac) via histone deacetylase 6 (HDAC6) regulation. Heat shock inhibits the interaction between HDAC6 and heat shock protein 90 (HSP90), enhances nuclear localization of HDAC6, and promotes HDAC6 phosphorylation, which is regulated by protein phosphatase 2A (PP2A). Combining hyperthermia with HDAC inhibitors vorinostat or panobinostat leads to better anti-cancer effects compared to monotherapy. KEAP1 and DPP7 as genes affected by heat-induced inhibition of H3K9ac, and combining them with hyperthermia can better induce apoptosis in tumor cells. This study reveals previously unknown mechanisms of H3K9ac decreased by heat shock in cancer cells and highlights a potential combinational therapy involving hyperthermia and targeting of these new mechanisms.

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Section: Resultsmentioning

confidence: 99%

Inhibition of Heat Shock-Induced H3K9ac Reduction Sensitizes Cancer Cells to Hyperthermia

Lin,

Song,

Song

et al. 2023

Int. J. Biol. Sci.

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“…ESI-MS m/z: 348 [M + H] + . [4,3-b]indole-2-carboxylate (9). To a mixture of 7c (200 mg, 0.46 mmol, 1.00 equiv) in THF (10 mL), K 2 CO 3 (318 mg, 2.31 mmol, 5.00 equiv) was added.…”

Section: ■ Conclusionmentioning

confidence: 99%

“…Recent neuroprotective approaches to RP target the epigenome and are based on the rationale that not only specific DNA mutations in retinal cells but also epigenetic changes contribute to the pathogenesis of the disease. 9 In particular, the DNA demethylation pathway is essential for photoreceptor specification, maturation, and function, so the unsuccessful demethylation of regulatory sequences during the differentiation of progenitor cells into photoreceptors may contribute to the development of RP. 10 As part of the epigenetic machinery, histone deacetylases (HDACs) have been shown to regulate gene expression, suppressing microglia-initiated inflammation and reducing photoreceptor loss in RP, preserving the visual function.…”

Section: ■ Introductionmentioning

confidence: 99%

Targeting Relevant HDACs to Support the Survival of Cone Photoreceptors in Inherited Retinal Diseases: Identification of a Potent Pharmacological Tool with In Vitro and In Vivo Efficacy

Carullo,

Orsini,

Piano

et al. 2024

J. Med. Chem.

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“…Int J Ophthalmol, Vol. 16 Histone deacetylases (HDACs) plays a crucial role in regulating the development of various retinal cells, including retinal progenitor cells, photoreceptors, bipolar cells, ganglion cells and Müller glial cells [11] . HDACs IIa (HDAC4/5/7/9) regulate many aspects of cell biology, including proliferation, differentiation, autophagy, apoptosis, migration and angiogenesis [12][13] .…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of histone deacetylase 7 reduces biological activities of retinal microvascular endothelial cells under high glucose condition and related mechanism

Ning¹,

Xie²,

Chen³

et al. 2023

Int J Ophthalmol

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AIM: To investigate the expression and effect of histone deacetylase 7 (HDAC7) in human retinal microvascular endothelial cells (HRMECs) under high glucose condition and related mechanism, and the expression of HDAC7 in the retinal tissue in diabetic rats. METHODS: The expression of HDAC7 in HRMECs under high glucose and the retinal tissue from normal or diabetic rats were detected with immunohistochemistry and Western blot. LV-shHDAC7 HRMECs were used to study the effect of HDAC7 on cell activities. Cell count kit-8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), flow cytometry, scratch test, Transwell test and tube formation assay were used to examine the ability of cell proliferation, migration, and angiogenesis. Finally, a preliminary exploration of its mechanism was performed by Western blot. RESULTS: The expression of HDAC7 was both up-regulated in retinal tissues of diabetic rats and high glucose-treated HRMECs. Down-regulation of HDAC7 expression significantly reduced the ability of proliferation, migration, and tube formation, and reversed the high glucose-induced high expression of CDK1/Cyclin B1 and vascular endothelial growth factor in high glucose-treated HRMECs. CONCLUSION: High glucose can up-regulate the expression of HDAC7 in HRMECs. Down-regulation of HDAC7 can inhibit HRMECs activities. HDAC7 is proposed to be involved in pathogenesis of diabetic retinopathy and a therapeutic target.

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Roles of Histone Acetyltransferases and Deacetylases in the Retinal Development and Diseases

Cited by 5 publications

References 194 publications

Inhibition of Heat Shock-Induced H3K9ac Reduction Sensitizes Cancer Cells to Hyperthermia

Inhibition of Heat Shock-Induced H3K9ac Reduction Sensitizes Cancer Cells to Hyperthermia

Targeting Relevant HDACs to Support the Survival of Cone Photoreceptors in Inherited Retinal Diseases: Identification of a Potent Pharmacological Tool with In Vitro and In Vivo Efficacy

Down-regulation of histone deacetylase 7 reduces biological activities of retinal microvascular endothelial cells under high glucose condition and related mechanism

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