Loss of Bone Morphogenetic Protein-9 Reduces Survival and Increases MMP Activity After Myocardial Infarction

Bhave, Shreyas; Esposito, Michele; Swain, Lija; Qiao, Xiaoying; Martin, Gregory; Wadhwa, Sakshi; Everett, Kay; Kapur, Navin K.

doi:10.1016/j.jacbts.2023.05.017

Cited by 2 publications

(1 citation statement)

References 37 publications

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“…In the MI scenario, heme oxygenase (hmox1) has been demonstrated to reduce infarct size and left ventricular remodeling in murine models of permanent ischemia [19], and exert cardioprotective effects via attenuating cardiomyocyte senescence [20], whereas midkine (mdk) administration prevents left ventricular remodeling by promoting angiogenesis and reducing collagen deposition and apoptosis activation [21]. Indeed, the loss of growth differentiation factor 2 (gdf2) promotes cardiac fibrosis, collagen degradation, and cardiac rupture after MI via metalloproteinase 9 [22]. Lastly, circulating levels of arginase 1 (arg1) are augmented in MI patients compared to the controls, and positively correlate with the gensini score [23].…”

Section: Changes In the Transcriptomic Expression Of The Genes Involv...mentioning

confidence: 99%

Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis

Ortega,

Molina-García,

Gavara

et al. 2023

IJMS

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Endothelial cells (ECs) are a key target for cardioprotection due to their role in preserving cardiac microvasculature and homeostasis after myocardial infarction (MI). Our goal is to identify the genes involved in post-MI EC proliferation, EC apoptosis, and angiogenesis regulation via RNA-sequencing transcriptomic datasets. Using eight studies from the Gene Expression Omnibus, RNA-sequencing data from 92 mice submitted to different times of coronary ischemia or sham were chosen. Functional enrichment analysis was performed based on gene ontology biological processes (BPs). Apoptosis-related BPs are activated up to day 3 after ischemia onset, whereas endothelial proliferation occurs from day 3 onwards, including an overrepresentation of up to 37 genes. Endothelial apoptosis post-MI is triggered via both the extrinsic and intrinsic signaling pathways, as reflected by the overrepresentation of 13 and 2 specific genes, respectively. BPs implicated in new vessel formation are upregulated soon after ischemia onset, whilst the mechanisms aiming at angiogenesis repression can be detected at day 3. Overall, 51 pro-angiogenic and 29 anti-angiogenic factors displayed altered transcriptomic expression post-MI. This is the first study using RNA sequencing datasets to evaluate the genes participating in post-MI endothelium physiology and angiogenesis regulation. These novel data could lay the groundwork to advance understanding of the implication of ECs after MI.

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Section: Changes In the Transcriptomic Expression Of The Genes Involv...mentioning

confidence: 99%

Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis

Ortega,

Molina-García,

Gavara

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

ALK1 Deficiency Impairs the Wound-Healing Process and Increases Mortality in Murine Model of Myocardial Infarction

Bhave,

Swain,

Qiao

et al. 2023

J. of Cardiovasc. Trans. Res.

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Loss of Bone Morphogenetic Protein-9 Reduces Survival and Increases MMP Activity After Myocardial Infarction

Cited by 2 publications

References 37 publications

Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis

Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis

ALK1 Deficiency Impairs the Wound-Healing Process and Increases Mortality in Murine Model of Myocardial Infarction

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