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Article ; Online: Transmembrane protein TMEM97 and epigenetic reader BAHCC1 constitute an axis that supports pro-inflammatory cytokine expression.

Li, Jing / Shen, Hongtao / Guo, Lian-Wang

2024 Volume 116, Page(s) 111069

Abstract: Pro-inflammatory cytokine production by the retinal pigment epithelium (RPE) is a key etiology in retinal degenerative diseases, yet the underlying mechanisms are not well understood. TMEM97 is a scarcely studied transmembrane protein recently implicated ...

Abstract	Pro-inflammatory cytokine production by the retinal pigment epithelium (RPE) is a key etiology in retinal degenerative diseases, yet the underlying mechanisms are not well understood. TMEM97 is a scarcely studied transmembrane protein recently implicated in retinal degeneration. BAH domain coiled coil 1 (BAHCC1) is a newly discovered histone code reader involved in oncogenesis. A role for TMEM97 and BAHCC1 in RPE inflammation was not known. Here we found that they constitute a novel axis regulating pro-inflammatory cytokine expression in RPE cells. Transcriptomic analysis using a TMEM97-/- ARPE19 human cell line and the validation via TMEM97 loss- and gain-of-function revealed a profound role of TMEM97 in promoting the expression of pro-inflammatory cytokines, notably IL1β and CCL2, and unexpectedly BAHCC1 as well. Moreover, co-immunoprecipitation indicated an association between the TMEM97 and BAHCC1 proteins. While TMEM97 ablation decreased and its overexpression increased NFκB (p50, p52, p65), the master transcription factor for pro-inflammatory cytokines, silencing BAHCC1 down-regulated NFκB and downstream pro-inflammatory cytokines. Furthermore, in an RPE-damage retinal degeneration mouse model, immunofluorescence illustrated down-regulation of IL1β and CCL2 total proteins and suppression of glial activation in the retina of Tmem97-/- mice compared to Tmem97+/+ mice. Thus, TMEM97 is a novel determinant of pro-inflammatory cytokine expression acting via a previously unknown TMEM97- > BAHCC1- > NFκB cascade. SYNOPSIS: Retinal pigment epithelium (RPE) inflammation can lead to blindness. We identify here a previously uncharacterized cascade that underlies RPE cell production of pro-inflammatory cytokines. Specifically, transmembrane protein TMEM97 positively regulates the recently discovered histone code reader BAHCC1, which in turn enhances pro-inflammatory cytokine expression via the transcription factor NFκB.
MeSH term(s)	Humans ; Mice ; Animals ; Cytokines/metabolism ; Retinal Degeneration/genetics ; Cells, Cultured ; Retina/metabolism ; Inflammation/metabolism ; Epigenesis, Genetic ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Proteins/metabolism
Chemical Substances	Cytokines ; TMEM97 protein, human ; Membrane Proteins ; BAHCC1 protein, human ; Proteins
Language	English
Publishing date	2024-01-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2024.111069
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Zs.A 2579: Show issues

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Article ; Online: Sphingoid Bases Regulate the Sigma-1 Receptor-Sphingosine and

Li, Jing / Satyshur, Kenneth A / Guo, Lian-Wang / Ruoho, Arnold E

International journal of molecular sciences

2023 Volume 24, Issue 4

Abstract: Both bioactive sphingolipids and Sigma-1 receptor (S1R) chaperones occur ubiquitously in mammalian cell membranes. Endogenous compounds that regulate the S1R are important for controlling S1R responses to cellular stress. Herein, we interrogated the S1R ... ...

Abstract	Both bioactive sphingolipids and Sigma-1 receptor (S1R) chaperones occur ubiquitously in mammalian cell membranes. Endogenous compounds that regulate the S1R are important for controlling S1R responses to cellular stress. Herein, we interrogated the S1R in intact Retinal Pigment Epithelial cells (ARPE-19) with the bioactive sphingoid base, sphingosine (SPH), or the pain-provoking dimethylated SPH derivative,
MeSH term(s)	Animals ; Sphingosine ; Sphingolipids ; Receptors, sigma ; Ceramides ; Mammals/metabolism ; Sigma-1 Receptor
Chemical Substances	Sphingosine (NGZ37HRE42) ; Sphingolipids ; Receptors, sigma ; Ceramides
Language	English
Publishing date	2023-02-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24043103
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Article: Correction: miR548ai antagonism attenuates exosome-induced endothelial cell dysfunction.

Xie, Xiujie / Guo, Lian-Wang / Kent, Craig K

Cell death discovery

2022 Volume 8, Issue 1, Page(s) 382

Language	English
Publishing date	2022-09-12
Publishing country	United States
Document type	Published Erratum
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-022-01178-z
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Article: SREBP1 regulates

Li, Jing / Shen, Hongtao / Owens, Gary K / Guo, Lian-Wang

Molecular therapy. Nucleic acids

2022 Volume 28, Page(s) 892–909

Abstract: Aberrant smooth muscle cell (SMC) plasticity is etiological to vascular diseases. Cholesterol induces SMC phenotypic transition featuring high LGALS3 (galectin-3) expression. This proatherogenic process is poorly understood for its molecular ... ...

Abstract	Aberrant smooth muscle cell (SMC) plasticity is etiological to vascular diseases. Cholesterol induces SMC phenotypic transition featuring high LGALS3 (galectin-3) expression. This proatherogenic process is poorly understood for its molecular underpinnings, in particular, the mechanistic role of sterol regulatory-element binding protein-1 (SREBP1), a master regulator of lipid metabolism. Herein we show that cholesterol loading stimulated SREBP1 expression in mouse, rat, and human SMCs. SREBP1 positively regulated LGALS3 expression (and vice versa), whereas Krüppel-like factor-15 (KLF15) acted as a negative regulator. Both bound to the
Language	English
Publishing date	2022-05-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2662631-7
ISSN	2162-2531
ISSN	2162-2531
DOI	10.1016/j.omtn.2022.05.028
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Article: miR548ai antagonism attenuates exosome-induced endothelial cell dysfunction.

Xie, Xiujie / Guo, Lian-Wang / Kent, Craig K

Cell death discovery

2021 Volume 7, Issue 1, Page(s) 318

Abstract: Endothelial cell (EC) and smooth muscle cell (SMC) are major cell types adjacent in the vascular wall. Recent progress indicates that their communication is crucial for vascular homeostasis and pathogenesis. In particular, dysfunctional (proliferative) ... ...

Abstract	Endothelial cell (EC) and smooth muscle cell (SMC) are major cell types adjacent in the vascular wall. Recent progress indicates that their communication is crucial for vascular homeostasis and pathogenesis. In particular, dysfunctional (proliferative) SMCs through exosomes can induce EC dysfunction (impaired growth). The current study suggests that miR548ai, a rarely known microRNA, may provide a molecular target for protection against SMC/exosome-induced EC dysfunction. We performed microarray profiling of microRNAs of dysfunctional human primary aortic SMCs induced by different cytokines (PDGF-BB, TGFβ1, TNFα, IL1β). Among the microRNAs commonly upregulated by these cytokines, miR548ai showed the most robust changes, as also validated through quantitative PCR. This cytokine-induced miR548ai upregulation was recapitulated in the qPCR determination of SMC-derived exosomal microRNAs. Consistent with SMC-to-EC communication, the exosomes extracted from cytokine-stimulated SMCs impaired human EC proliferation and migration. Of particular interest, this SMC exosomal impingement on ECs was countered by transfection of miR548ai inhibitor microRNA into ECs. Furthermore, the miR548ai inhibitor transfected into SMCs attenuated SMC dysfunction/proliferation. Thus, these results identify miR548ai as a novel target; namely, miR548ai inhibitor mitigates EC dysfunction induced by exosomes derived from dysfunctional SMCs. This new knowledge may aid the future development of microRNA-based treatment of vascular disorders.
Language	English
Publishing date	2021-10-28
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-021-00720-9
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Article: miR579-3p is an inhibitory modulator of neointimal hyperplasia and transcription factors c-MYB and KLF4.

Xie, Xiujie / Shirasu, Takuro / Li, Jing / Guo, Lian-Wang / Kent, K Craig

Cell death discovery

2023 Volume 9, Issue 1, Page(s) 73

Abstract: Neointimal hyperplasia (IH) is a common vascular pathology that typically manifests in in-stent restenosis and bypass vein graft failure. Smooth muscle cell (SMC) phenotypic switching is central to IH, both regulated by some microRNAs, yet the role of ... ...

Abstract	Neointimal hyperplasia (IH) is a common vascular pathology that typically manifests in in-stent restenosis and bypass vein graft failure. Smooth muscle cell (SMC) phenotypic switching is central to IH, both regulated by some microRNAs, yet the role of miR579-3p, a scarcely studied microRNA, is not known. Unbiased bioinformatic analysis suggested that miR579-3p was repressed in human primary SMCs treated with different pro-IH cytokines. Moreover, miR579-3p was software-predicted to target both c-MYB and KLF4 - two master transcription factors known to promote SMC phenotypic switching. Interestingly, treating injured rat carotid arteries via local infusion of miR579-3p-expressing lentivirus reduced IH 14 days after injury. In cultured human SMCs, transfection with miR579-3p inhibited SMC phenotypic switching, as indicated by decreased proliferation/migration and increased SMC contractile proteins. miR579-3p transfection downregulated c-MYB and KLF4, and luciferase assays indicated miR579-3p's targeting of the 3'UTRs of the c-MYB and KLF4 mRNAs. In vivo, immunohistochemistry showed that treatment of injured rat arteries with the miR579-3p lentivirus reduced c-MYB and KLF4 and increased SMC contractile proteins. Thus, this study identifies miR579-3p as a previously unrecognized small-RNA inhibitor of IH and SMC phenotypic switch involving its targeting of c-MYB and KLF4. Further studies on miR579-3p may provide an opportunity for translation to develop IH-mitigating new therapeutics.
Language	English
Publishing date	2023-02-22
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-023-01364-7
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Article ; Online: Signaling Mechanisms of Myofibroblastic Activation: Outside-in and Inside-Out.

Zent, Joshua / Guo, Lian-Wang

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2018 Volume 49, Issue 3, Page(s) 848–868

Abstract: Myofibroblasts are central mediators of fibrosis. Typically derived from resident fibroblasts, myofibroblasts represent a heterogeneous population of cells that are principally defined by acquired contractile function and high synthetic ability to ... ...

Abstract	Myofibroblasts are central mediators of fibrosis. Typically derived from resident fibroblasts, myofibroblasts represent a heterogeneous population of cells that are principally defined by acquired contractile function and high synthetic ability to produce extracellular matrix (ECM). Current literature sheds new light on the critical role of ECM signaling coupled with mechanotransduction in driving myofibroblastic activation. In particular, transforming growth factor β1 (TGF-β1) and extra domain A containing fibronectin (EDA-FN) are thought to be the primary ECM signaling mediators that form and also induce positive feedback loops. The outside-in and inside-out signaling circuits are transmitted and integrated by TGF-β receptors and integrins at the cell membrane, ultimately perpetuating the abundance and activities of TGF-β1 and EDA-FN in the ECM. In this review, we highlight these conceptual advances in understanding myofibroblastic activation, in hope of revealing its therapeutic anti-fibrotic implications.
MeSH term(s)	Extracellular Matrix/metabolism ; Fibronectins/metabolism ; Focal Adhesions/metabolism ; Humans ; Integrins/metabolism ; Mechanotransduction, Cellular ; Myofibroblasts/metabolism ; Signal Transduction ; Transforming Growth Factor beta1/metabolism ; rho GTP-Binding Proteins/metabolism
Chemical Substances	Fibronectins ; Integrins ; Transforming Growth Factor beta1 ; extra domain A fibronectin, human ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2018-09-05
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000493217
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Zs.A 3160: Show issues

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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: BET Epigenetic Reader Proteins in Cardiovascular Transcriptional Programs.

Borck, Patricia Cristine / Guo, Lian-Wang / Plutzky, Jorge

Circulation research

2020 Volume 126, Issue 9, Page(s) 1190–1208

Abstract: Epigenetic mechanisms involve the placing (writing) or removal (erasing) of histone modifications that allow heterochromatin to transition to the open, activated euchromatin state necessary for transcription. A third, less studied epigenetic pathway ... ...

Abstract	Epigenetic mechanisms involve the placing (writing) or removal (erasing) of histone modifications that allow heterochromatin to transition to the open, activated euchromatin state necessary for transcription. A third, less studied epigenetic pathway involves the reading of these specific histone marks once placed. The BETs (bromodomain and extraterminal-containing protein family), which includes BRD2, BRD3, and BRD4 and the testis-restricted BRDT, are epigenetic reader proteins that bind to specific acetylated lysine residues on histone tails where they facilitate the assembly of transcription complexes including transcription factors and transcriptional machinery like RNA Polymerase II. As reviewed here, considerable recent data establishes BETs as novel determinants of induced transcriptional programs in vascular cells, like endothelial cells and vascular smooth muscle cells, cardiac myocytes and inflammatory cells, like monocyte/macrophages, cellular settings where these epigenetic reader proteins couple proximal stimuli to chromatin, acting at super-enhancer regulatory regions to direct gene expression. BET inhibition, including the use of specific chemical BET inhibitors like JQ-1, has many reported effects in vivo in the cardiovascular setting, like decreasing atherosclerosis, angiogenesis, intimal hyperplasia, pulmonary arterial hypertension, and cardiac hypertrophy. At the same time, data in endothelial cells, adipocytes, and elsewhere suggest BETs also help regulate gene expression under basal conditions. Studies in the cardiovascular setting have highlighted BET action as a means of controlling gene expression in differentiation, cell identity, and cell state transitions, whether physiological or pathological, adaptive, or maladaptive. While distinct BET inhibitors are being pursued as therapies in oncology, a large prospective clinical cardiovascular outcome study investigating the BET inhibitor RVX-208 (now called apabetalone) has already been completed. Independent of this specific agent and this one trial or the numerous unanswered questions that remain, BETs have emerged as novel epigenetic players involved in the execution of coordinated transcriptional programs in cardiovascular health and disease.
MeSH term(s)	Acetylation ; Animals ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Chromatin Assembly and Disassembly/drug effects ; Epigenesis, Genetic/drug effects ; Histones/metabolism ; Humans ; Quinazolinones/therapeutic use ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects
Chemical Substances	Histones ; Quinazolinones ; Transcription Factors ; apabetalone (8R4A7GDZ1D)
Language	English
Publishing date	2020-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.120.315929
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Article ; Online: Smad2 inhibition of

Xie, Xiujie / Shirasu, Takuro / Guo, Lian-Wang / Kent, K Craig

Atherosclerosis plus

2021 Volume 44, Page(s) 31–42

Abstract: Background: Vascular smooth muscle cell (SMC) apoptosis is involved in major cardiovascular diseases. Smad2 is a transcription factor implicated in aortic aneurysm. The molecular mediators of Smad2-driven SMC apoptosis are not well defined. Here we have ...

Abstract	Background: Vascular smooth muscle cell (SMC) apoptosis is involved in major cardiovascular diseases. Smad2 is a transcription factor implicated in aortic aneurysm. The molecular mediators of Smad2-driven SMC apoptosis are not well defined. Here we have identified a Smad2-directed mechanism involving Methods and results: Guided by microarray analysis in human primary aortic SMCs, loss/gain-of-function (siRNA/overexpression) indicated that Smad2 negatively and positively regulated, respectively, the gene expression of Met which was identified herein as anti-apoptotic and that of Fas, Conclusions: Our study suggests a pro-apoptotic mechanism in human SMCs, whereby Smad2 negatively and positively regulates
Language	English
Publishing date	2021-08-21
Publishing country	Netherlands
Document type	Journal Article
ISSN	2667-0895
ISSN (online)	2667-0895
DOI	10.1016/j.athplu.2021.08.005
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Article: Peeking into Sigma-1 Receptor Functions Through the Retina.

Mavlyutov, Timur A / Guo, Lian-Wang

Advances in experimental medicine and biology

2017 Volume 964, Page(s) 285–297

Abstract: This review discusses recent advances towards understanding the sigma-1 receptor (S1R) as an endogenous neuro-protective mechanism in the retina , a favorable experimental model system. The exquisite architecture of the mammalian retina features layered ... ...

Abstract	This review discusses recent advances towards understanding the sigma-1 receptor (S1R) as an endogenous neuro-protective mechanism in the retina , a favorable experimental model system. The exquisite architecture of the mammalian retina features layered and intricately wired neurons supported by non-neuronal cells. Ganglion neurons, photoreceptors , as well as the retinal pigment epithelium, are susceptible to degeneration that leads to major retinal diseases such as glaucoma , diabetic retinopathy , and age-related macular degeneration (AMD), and ultimately, blindness. The S1R protein is found essentially in every retinal cell type, with high abundance in the ganglion cell layer. Ultrastructural studies of photoreceptors, bipolar cells, and ganglion cells show a predominant localization of S1R in the nuclear envelope. A protective role of S1R for ganglion and photoreceptor cells is supported by in vitro and in vivo experiments. Most recently, studies suggest that S1R may also protect retinal neurons via its activities in Müller glia and microglia. The S1R functions in the retina may be attributed to a reduction of excitotoxicity, oxidative stress , ER stress response, or inflammation. S1R knockout mice are being used to delineate the S1R-specific effects. In summary, while significant progress has been made towards the objective of establishing a S1R-targeted paradigm for retinal neuro-protection , critical questions remain. In particular, context-dependent effects and potential side effects of interventions targeting S1R need to be studied in more diverse and more clinically relevant animal models.
MeSH term(s)	Animals ; Neuroprotective Agents/pharmacology ; Photoreceptor Cells/drug effects ; Photoreceptor Cells/metabolism ; Receptors, sigma/metabolism ; Retina/drug effects ; Retina/metabolism ; Retinal Diseases/drug therapy ; Retinal Diseases/metabolism ; Retinal Ganglion Cells/drug effects ; Retinal Ganglion Cells/metabolism ; Retinal Neurons/drug effects ; Retinal Neurons/metabolism ; Sigma-1 Receptor
Chemical Substances	Neuroprotective Agents ; Receptors, sigma
Language	English
Publishing date	2017-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	410187-X
ISSN	0065-2598
ISSN	0065-2598
DOI	10.1007/978-3-319-50174-1_19
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