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Kindlin -2 is Essential for Preserving Integrity of the Developing Heart and Preventing Ventricular Rupture

ABSTRACT: Kindlin -2 is Essential for Preserving Integrity of the Developing Heart and Preventing Ventricular Rupture

PROVIDER: PRJNA508090 | ENA |

REPOSITORIES: ENA

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Kindlin -2 is Essential for Preserving Integrity of the Developing Heart and Preventing Ventricular Rupture

Project description:Using RNA sequencing we compared the transcriptome change between control and kindlin2 knockout heart samples

2018-12-04 | GSE123280 | GEO

Comparative therapeutic strategies for preventing aortic rupture in a mouse model of vascular Ehlers-Danlos syndrome

Project description:Comparative therapeutic strategies for preventing aortic rupture in a mouse model of vascular Ehlers-Danlos syndrome

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Comparative therapeutic strategies for preventing aortic rupture in a mouse model of vascular Ehlers-Danlos syndrome

Project description:Vascular Ehlers-Danlos syndrome is a rare inherited disorder caused by genetic variants in type III collagen. Its prognosis is especially hampered by unpredictable arterial ruptures and there is no therapeutic consensus. We created a knock-in Col3a1+/G182R mouse model and performed a complete genetic, molecular and biochemical characterization. Several therapeutic strategies were also tested. Col3a1+/G182R mice showed a spontaneous mortality caused by thoracic aortic rupture that recapitulates the vascular Ehlers-Danlos syndrome with a lower survival rate in males, thin non-inflammatory arteries and an altered arterial collagen. Transcriptomic analysis of aortas showed upregulation of genes related to inflammation and cell stress response. Compared to water, survival rate of Col3a1+/G182R mice was not affected by beta-blockers (propranolol or celiprolol). Two other vasodilating anti-hypertensive agents (hydralazine, amlodipine) gave opposite results on aortic rupture and mortality rate. There was a spectacular beneficial effect of losartan, reversed by the cessation of its administration, and a marked deleterious effect of exogenous angiotensin II. These results suggest that blockade of the renin angiotensin system should be tested as a first-line medical therapy in patients with vascular Ehlers-Danlos syndrome.

2022-02-16 | GSE196753 | GEO

NRG-1 induces mature ventricular cardiac differentiation from iPS cells contributing to cardiac tissue repair

Project description:Combined treatment with NRG-1 and DMSO led to efficient differentiation of iPS into mature ventricular-like cardiac cells, which were capable of preserving cardiac function and tissue viability when transplanted into a mouse model of myocardial infarction.

2017-03-24 | GSE56511 | GEO

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Transcriptional profiling of neonatal cord blood from babies born with or without prolonged rupture of membranes.

Project description:Prolonged rupture of membranes (PROM) is thought to incur higher risk of neonatal infection, leading to expedited delivery and/or the use of empirical perinatal antibiotics. Here, we compared the transcriptional profile of neonatal cord blood between babies where rupture of membranes occurred greater than 24 hours before delivery (= PROM cases) and babies where rupture of membranes occurred less than 24 hours before delivery (= Control cases). On the basis that perinatal infection is more likely in births associated with PROM than those without, we tested the hypothesis that perinatal infection in a subset of births following PROM, exhibit immune responses evident in the neonatal cord blood transcriptome.

2018-12-20 | E-MTAB-6431 | biostudies-arrayexpress

Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

Project description:Left ventricular noncompaction (LVNC) Causes prominent ventricular trabeculations and reduces cardiac systolic function. The clinical presentation of LVNC ranges from asymptomatic to heart failure. We show that germline mutations in human MIB1 (mindbomb homolog 1), which encodes an E3 ubiquitin ligase that promotes endocytosis of the NOTCH ligands DELTA and JAGGED, cause LVNC in autosomal-dominant pedigrees, with affected individuals showing reduced NOTCH1 activity and reduced expression of target genes. Functional studies in cells and zebrafish embryos and in silico modeling indicate that MIB1 functions as a dimer, which is disrupted by the human mutations. Targeted inactivation of Mib1 in mouse myocardium causes LVNC, a phenotype mimicked by inactivation of myocardial Jagged1 or endocardial Notch1. Myocardial Mib1 mutants show reduced ventricular Notch1 activity, expansion of compact myocardium to proliferative, immature trabeculae and abnormal expression of cardiac development and disease genes. These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. RNA was isolated from the ventricles of 16 WT and 16 Mib1flox; CTnT-cre hearts at E14.5 and then pooled into four replicates.

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Expression data of cDNA from the ACHN control and Kindlin-2-depleting cells

Project description:Kindlin-2, an integrin-interacting FERM-domain-containing protein, has been known to play critical roles for tumor progression. However, the role of Kindlin-2 in renal cell carcinoma (RCC) progression has not been reported. We aim to investigate the role of Kindlin-2 in the progression of RCC and the underlying mechanisms. To uncover the related pathway in which Kindlin-2 is involved to promote clear cell renal cell carcinoma progression, ACHN control and Kindlin-2-depleting cells were analyzed by Affymetrix GeneChip human Gene 1.0 ST Arrays. ACHN cells were transfected with control short hairpin RNA (shRNA) or Kindlin-2 shRNA. ACHN control and Kindlin-2-depleting cells cDNAs were hybridized to Affymetrix GeneChip Human Gene 1.0 ST arrays. Data were analyzed by Expression Console 1.4.1.

2015-12-16 | E-GEOD-76020 | biostudies-arrayexpress

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Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

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