RhoB antibody alters retinal vascularization in models of murine retinopathy

Almonte-Baldonado, Rowena; Bravo‐Nuevo, Arturo; Gerald, Damien; Benjamin, Laura E.; Prendergast, George C.; Laury‐Kleintop, Lisa D.

doi:10.1002/jcb.28213

Cited by 4 publications

(2 citation statements)

References 39 publications

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“…A recent study has shown that hypoxia significantly upregulates the expression of RHOB (Huang et al, 2017). Concurrent studies suggested that RHOB was genetically required for pathogenic retinal angiogenesis (Almonte-Baldonado et al, 2019). Likewise, RHOB was also up-regulated in AAK patients.…”

Section: Discussionmentioning

confidence: 97%

Construction of ceRNA network and identification of hub genes in aniridia-associated keratopathy using bioinformatics analysis

Zhang²,

Wu³

et al. 2022

Front. Genet.

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Aniridia-associated keratopathy (AAK) is characteristic at ocular surface of aniridia caused by haploinsufficiency of PAX6. Competing endogenous RNA (ceRNA) has been reported to play an important role in various diseases, whereas its function on AAK is unclear. The microarray data of 20 AAK patients and 20 healthy people were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed lncRNAs, miRNAs, and mRNAs were analyzed using “limma” packages and weighted gene co-expression network analysis (WGCNA). A ceRNA network was constructed by Cytoscape 3.9.1, and miR-224-5p, miR-30a-5p, and miR-204-5p were at the center of the network. CIBERSORTx algorithm and ssGSEA analyses revealed that AAK was associated with immune cell infiltration, showing that activated Mast cells increased while resting Mast cells decreased and NK cells decreased in AAK. Type II INF Response, CCR, parainflammation, T cell co-stimulation, and APC co-stimulation of AAK patients differed from healthy individuals. Additionally, the ROC curve of five genes, MITF(AUC = 0.988), RHOB(AUC = 0.973), JUN(AUC = 0.953), PLAUR (AUC = 0.925), and ARG2 (AUC = 0.915) with high confidence in predicting AAK were identified. Gene set enrichment analysis (GSEA) analysis of hub genes enriched in the IL-17 signaling pathway.

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Section: Discussionmentioning

confidence: 97%

Construction of ceRNA network and identification of hub genes in aniridia-associated keratopathy using bioinformatics analysis

Zhang²,

Wu³

et al. 2022

Front. Genet.

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“…Increased RhoB transcription is associated with the disruptive effects of celiac patient antibodies on angiogenesis [83] and RhoB-null mice have decreased pathological angiogenesis in the ischemic retina, suggesting an important role in disease-specific angiogenesis [46] (Figure 4). Excitingly, an antibody against RhoB decreases angiogenesis in a model of proliferative retina angiogenesis and oxygen-induced retinopathy in an early pre-clinical study, suggesting that RhoB may not be required for vessel maintenance and could be specific to pathogenic vessels [84]. RhoB could represent an exciting new target for disease treatment in which blockage of abnormal angiogenesis, rather than angiogenesis as a whole, is desirable.…”

Section: Angiogenesismentioning

confidence: 99%

Building Blood Vessels—One Rho GTPase at a Time

Barlow

Cleaver

2019

Cells

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Blood vessels are required for the survival of any organism larger than the oxygen diffusion limit. Blood vessel formation is a tightly regulated event and vessel growth or changes in permeability are linked to a number of diseases. Elucidating the cell biology of endothelial cells (ECs), which are the building blocks of blood vessels, is thus critical to our understanding of vascular biology and to the development of vascular-targeted disease treatments. Small GTPases of the Rho GTPase family are known to regulate several processes critical for EC growth and maintenance. In fact, many of the 21 Rho GTPases in mammals are known to regulate EC junctional remodeling, cell shape changes, and other processes. Rho GTPases are thus an attractive target for disease treatments, as they often have unique functions in specific vascular cell types. In fact, some Rho GTPases are even expressed with relative specificity in diseased vessels. Interestingly, many Rho GTPases are understudied in ECs, despite their known expression in either developing or mature vessels, suggesting an even greater wealth of knowledge yet to be gleaned from these complex signaling pathways. This review aims to provide an overview of Rho GTPase signaling contributions to EC vasculogenesis, angiogenesis, and mature vessel barrier function. A particular emphasis is placed on so-called “alternative” Rho GTPases, as they are largely understudied despite their likely important contributions to EC biology.

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RhoB Promotes Endometrial Stromal Cells Decidualization Via Semaphorin3A/PlexinA4 Signaling in Early Pregnancy

Zhao

et al. 2022

Endocrinology

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Endometrial decidualization refers to a series of morphological changes and functional remodeling of the uterine endometrium to accept the embryo under the effect of estrogen and progesterone secreted by ovaries after ovulation. During decidualization, endometrial stromal cells (ESCs) proliferate and differentiate into decidual stromal cells (DSCs), undergoing cytoskeletal rearrangement-mediated morphological changes and expressing decidualization markers, such as insulin-like growth factor-binding protein-1 (IGFBP1) and prolactin (PRL). Ras homology (Rho) proteins, a family of small G proteins, are well-known as regulators of cellular morphology and involved in multiple other cellular processes. In this study, we found ras homolog family member B (RHOB) was the most significantly upregulated gene in Rho protein family after the in vitro decidualization of human primary ESCs. RhoB expression was induced mainly by cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-response element binding protein (CREB) signaling and partly by progesterone signaling. Knockdown of RhoB in ESCs greatly inhibited actin cytoskeletal rearrangement, cell morphological transformation and upregulation of IGFBP1, suggesting an indispensable role of RhoB in decidualization. Mechanistically, the downstream target of RhoB was Semaphorin3A (Sema3A) which mediated its signaling via interacting with the receptor, plexinA4. More importantly, decreased expression of RhoB, Sema3A and plexinA4 were detected in deciduas from patients with unexplained spontaneous miscarriage. Collectively, our results indicate that RhoB/Sema3A/plexinA4 signaling plays a positive role in endometrial decidualization and relates to unexplained spontaneous miscarriage, which is worthy of further exploration so as to provide new insights into therapeutic strategies for pregnancy diseases associated with poor decidualization.

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RhoB antibody alters retinal vascularization in models of murine retinopathy

Cited by 4 publications

References 39 publications

Construction of ceRNA network and identification of hub genes in aniridia-associated keratopathy using bioinformatics analysis

Construction of ceRNA network and identification of hub genes in aniridia-associated keratopathy using bioinformatics analysis

Building Blood Vessels—One Rho GTPase at a Time

RhoB Promotes Endometrial Stromal Cells Decidualization Via Semaphorin3A/PlexinA4 Signaling in Early Pregnancy

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