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Lentiviral-mediated small hairpin RNAs (shRNAs)-based knockdown of OLFM2 or PKP2 in human adipocytes

ABSTRACT: We introduced into subcutaneous fully-differentiated human adipocytes from the same subject small hairpin RNAs (shRNAs) against two genes, thus enabling the study of functional consequences of sustained OLFM2 (shOLFM2; n=3 biological replicates) and PKP2 (shPKP2; n=3) knockdown in these cells. The lentiviral-based transfection was used to provide a long-lasting, convenient, reliable and efficient knockdown into in vitro cultured and fully differentiated adipocytes maintained for 6 d after reaching fully differentiation. A non-targeting shRNA was used as control (shCTRL; n=4) and reference for both modifications.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182229 | GEO | 2021/12/28

REPOSITORIES: GEO

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Short interfering RNAs (siRNAs)-based knockdown of OLFM2 or PKP2 in human adipocytes

Project description:We introduced into subcutaneous fully-differentiated human adipocytes from the same subject short interfering RNAs (siRNAs), thus enabling the study of functional consequences of OLFM2 (siOLFM2; n=3 biological replicates) and PKP2 (siPKP2; n=3) knockdown in these cells. A lipid-based transfection reagent (i.e. Lipofectamine 3000 reagent) was used to provide a transient (72h), convenient, reliable and efficient transfection into in vitro cultured and fully differentiated adipocytes. A non-targeting siRNA was used as control (siCTRL; n=4) for both modifications.

2021-12-28 | GSE182231 | GEO

Lentiviral-mediated small hairpin RNAs (shRNAs)-based knockdown of OLFM2 or PKP2 in human adipocytes

Project description:Lentiviral-mediated small hairpin RNAs (shRNAs)-based knockdown of OLFM2 or PKP2 in human adipocytes

| PRJNA755335 | ENA

Short interfering RNAs (siRNAs)-based knockdown of OLFM2 or PKP2 in human adipocytes

Project description:Short interfering RNAs (siRNAs)-based knockdown of OLFM2 or PKP2 in human adipocytes

| PRJNA755338 | ENA

To explore the downstream genes of PKP2

Project description:To explore the downstream genes of PKP2,we performed RNA-seq to screen after overexpression of PKP2 in A549 cells.

2023-08-05 | GSE155759 | GEO

Loss of the armadillo-repeat protein Plakophilin 2 in obesity breaks cell cycle dynamics to breed adipocyte senescence

Project description:Plakophilin2 (PKP2) is a key component of desmosomes mostly recognized for its involvement in the fibro fatty infiltration of heart muscle under defective PKP2. While thoroughly explored in cardiomyocytes, less attention has been given to its role in fat cells. Here we report steadily increased PKP2 during adipogenesis, with expression levels reaching its apex in terminally differentiated adipocytes. Notably, the loss of this protein in adipocytes under a pro-inflammatory microenvironment demonstrates its commitment in maintaining the expression of genes required to nurture cell cycle. Then, we show that diminished expressions of this member of the armadillo repeat family in subcutaneous adipose tissue co-segregate with obesity, being normalized upon mild to intense weight loss. We also demonstrate that impaired PKP2 in human adipocytes breaks cell cycle dynamics to breed premature senescence, a key rheostat for stress induced adipose tissue dysfunction. Conversely, restoring PKP2 in inflamed adipocytes rewires E2F signalling towards re-activation of cell cycle and decreased senescence. Our findings bound the expression of PKP2 in fat cells to the physiopathology of obesity, and uncover a previously unknown defect in cell cycle and activated adipocyte senescence due to impaired PKP2.

2023-05-10 | MSV000091898 | MassIVE

TNYA0016: Time-dependent transcriptional effects of PKP2 mRNA knockdown in wild-type human iPSC-CMs

Project description:Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a familial cardiac disease associated with ventricular arrhythmias and an increased risk of sudden cardiac death. Currently, there are no approved treatments that address the underlying genetic cause of this disease, representing a significant unmet need. Mutations in Plakophilin-2 (PKP2), encoding a desmosomal protein, account for approximately 40% of ARVC cases and result in reduced gene expression. Methods: Our goal is to examine the feasibility and the efficacy of adeno-associated virus 9 (AAV9)-mediated restoration of PKP2 expression in a cardiac specific knock-out mouse model of Pkp2. Results: We show that a single dose of AAV9:PKP2 gene delivery prevents disease development before the onset of cardiomyopathy and attenuates disease progression after overt cardiomyopathy. Restoration of PKP2 expression leads to a significant extension of lifespan by restoring cellular structures of desmosomes and gap junctions, preventing or halting decline in left ventricular ejection fraction, preventing or reversing dilation of the right ventricle, ameliorating ventricular arrhythmia event frequency and severity, and preventing adverse fibrotic remodeling. RNA sequencing analyses show that restoration of PKP2 expression leads to highly coordinated and durable correction of PKP2-associated transcriptional networks beyond desmosomes, revealing a broad spectrum of biological perturbances behind ARVC disease etiology. Conclusions: We identify fundamental mechanisms of PKP2-associated ARVC beyond disruption of desmosome function. The observed PKP2 dose-function relationship indicates that cardiac-selective AAV9:PKP2 gene therapy may be a promising therapeutic approach to treat ARVC patients with PKP2 mutations.

2024-02-23 | GSE253223 | GEO

TNYA0042: TN-401 dose-dependent efficacy study at about 10 weeks in Pkp2-cKO ARVC mouse model

2024-02-23 | GSE253224 | GEO

TNYA0044: AAV9:mPkp2 preventive vs therapeutic modes of treatment at 51 weeks in Pkp2-cKO ARVC mouse model

2024-02-23 | GSE253225 | GEO

Exploring the downstream genes of PKP2

Project description:Plakophilin 2 (PKP2), encodes a plakophilin protein that belongs to the member of desmosomal proteins.PkP2 regulates some cell biological functions, but its downstream genes are not clear, so we constructed a stable cell line using H460 cells and identified its downstream target genes by RNA-seq technology

2022-11-13 | GSE140509 | GEO

Human Long Intergenic Noncoding RNA Linc-ADAL Knockdown in Mature Adipocytes using Lentiviral ShRNA

Project description:Thousands of human long intergenic noncoding RNAs (lincRNAs) have been detected in human adipose tissue. Here we characterized the function of one human adipse lincRNA, linc-ADAL (chr5:115292235-115296985) in mature adipcoytes through loss-of-function studies. Our results indicate that knockdown of linc-ADAL in differentiated adipocytes modulated expression of lipid metabolism genes.

2019-02-13 | GSE95173 | GEO

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