Response Gene to Complement 32 in Vascular Diseases

Cui, Xiaobing; Chen, Shiyou

doi:10.3389/fcvm.2018.00128

Cited by 10 publications

(8 citation statements)

References 32 publications

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“…S19). Dysregulation of genes encoding factors involved in EC fate, blood vessel development, and angiogenesis (NOTCH4, FLT1, FGFR1, and RGCC) (42)(43)(44) in disease LVs indicated that vascular remodeling was a common heart failure feature.…”

Section: Endothelial Cellsmentioning

confidence: 99%

Pathogenic variants damage cell composition and single cell transcription in cardiomyopathies

Reichart

Lindberg

Maatz

et al. 2022

Science

128

138

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Pathogenic variants in genes that cause dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM) convey high risks for the development of heart failure through unknown mechanisms. Using single-nucleus RNA sequencing, we characterized the transcriptome of 880,000 nuclei from 18 control and 61 failing, nonischemic human hearts with pathogenic variants in DCM and ACM genes or idiopathic disease. We performed genotype-stratified analyses of the ventricular cell lineages and transcriptional states. The resultant DCM and ACM ventricular cell atlas demonstrated distinct right and left ventricular responses, highlighting genotype-associated pathways, intercellular interactions, and differential gene expression at single-cell resolution. Together, these data illuminate both shared and distinct cellular and molecular architectures of human heart failure and suggest candidate therapeutic targets.

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Section: Endothelial Cellsmentioning

confidence: 99%

Pathogenic variants damage cell composition and single cell transcription in cardiomyopathies

Reichart

Lindberg

Maatz

et al. 2022

Science

128

138

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“…We identified an epitope with a relatively large sequence (39AA) with homology to response gene to complement 32 (RGC32). RGC32 is induced by p53 in response to DNA damage and expressed in various tissues and is involved in numerous physiological and pathological processes, including cell proliferation, differentiation, fibrosis, metabolic disease [ 65 ]. The corresponding gene is involved in aniogenesis and regulated through hypoxia response element [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

Autoantibodies against cytoskeletons and lysosomal trafficking discriminate sarcoidosis from healthy controls, tuberculosis and lung cancers

et al. 2022

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Sarcoidosis is a systemic granulomatous disease of unknown etiology. Hypergammaglobulinemia and the presence of autoantibodies in sarcoidosis suggest active humoral immunity to unknown antigen(s). We developed a complex cDNA library derived from tissues of sarcoidosis patients. Using a high throughput method, we constructed a microarray platform from this cDNA library containing large numbers of sarcoidosis clones. After selective biopanning, 1070 sarcoidosis-specifc clones were arrayed and immunoscreend with 152 sera from patients with sarcoidosis and other pulmonary diseases. To identify the sarcoidosis classifiers two statistical approaches were conducted: First, we identified significant biomarkers between sarcoidosis and healthy controls, and second identified markers comparing sarcoidosis to all other groups. At the threshold of an False Discovery Rate (FDR) < 0.01, we identified 14 clones in the first approach and 12 clones in the second approach discriminating sarcoidosis from other groups. We used the classifiers to build a naïve Bayes model on the training-set and validated it on an independent test-set. The first approach yielded an AUC of 0.947 using 14 significant clones with a sensitivity of 0.93 and specificity of 0.88, whereas the AUC of the second option was 0.92 with a sensitivity of 0.96 and specificity of 0.83. These results suggest robust classifier performance. Furthermore, we characterized the informative phage clones by sequencing and homology searches. Large numbers of classifier-clones were peptides involved in cellular trafficking and cytoskeletons. These results show that sarcoidosis is associated with a specific pattern of immunoreactivity that can discriminate it from other diseases.

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“…Due to its roles in modulating cell cycle progression that were discovered in the past decades, it was renamed as regulator of cell cycle ( RGCC ) (Counts & Mufson, 2017). RGCC has been reported to regulate multiple cellular processes in various tissues such as kidney (Guo et al , 2011; Li et al , 2011), liver and adipose tissue (Cui et al , 2015), nervous system (Counts & Mufson, 2017; Kim & Park, 2019; Vlaicu et al , 2019), smooth muscle, and heart (Vlaicu et al , 2016) and has been implicated in many pathologic conditions, including cardiovascular (Cui & Chen, 2018), metabolic (Cui et al , 2015), renal (Li et al , 2011; Niu et al , 2011), autoimmune (Sun & Chen, 2018; Kim & Park, 2019), and neurodegenerative diseases (Counts & Mufson, 2017), as well as several cancers (Fosbrink et al , 2005; Vlaicu et al , 2010; Zhu et al , 2012; Sun et al , 2013; Xu et al , 2014). However, the roles of RGCC vary in different tissues and pathological processes.…”

Section: Discussionmentioning

confidence: 99%

RGCC balances self‐renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex

et al. 2021

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During neocortical development, neural stem cells (NSCs) divide symmetrically to self‐renew at the early stage and then divide asymmetrically to generate post‐mitotic neurons. The molecular mechanisms regulating the balance between NSC self‐renewal and neurogenesis are not fully understood. Using mouse in utero electroporation (IUE) technique and in vitro human NSC differentiation models including cerebral organoids (hCOs), we show here that regulator of cell cycle (RGCC) modulates NSC self‐renewal and neuronal differentiation by affecting cell cycle regulation and spindle orientation. RGCC deficiency hampers normal cell cycle process and dysregulates the mitotic spindle, thus driving more cells to divide asymmetrically. These modulations diminish the NSC population and cause NSC pre‐differentiation that eventually leads to brain developmental malformation in hCOs. We further show that RGCC might regulate NSC spindle orientation by affecting the organization of centrosome and microtubules. Our results demonstrate that RGCC is essential to maintain the NSC pool during cortical development and suggest that RGCC defects could have etiological roles in human brain malformations.

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Response Gene to Complement 32 in Vascular Diseases

Cited by 10 publications

References 32 publications

Pathogenic variants damage cell composition and single cell transcription in cardiomyopathies

Pathogenic variants damage cell composition and single cell transcription in cardiomyopathies

Autoantibodies against cytoskeletons and lysosomal trafficking discriminate sarcoidosis from healthy controls, tuberculosis and lung cancers

RGCC balances self‐renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex

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