ArticleFrontiers in physiology2016
Ablation of Matrix Metalloproteinase-9 Prevents Cardiomyocytes Contractile Dysfunction in Diabetics.
Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Mesenchymal stem-derived exosomes enhance therapeutic benefits of exercise in isoproterenol-induced myocardial ischemia: Targeting ERK and Akt/mTOR signaling.World journal of stem cells · 2025Article
- Matrix Metallopeptidase 9 Promotes Contraction in Human Uterine Myometrium.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2024Review
- Duality of Nrf2 in iron-overload cardiomyopathy.Haematologica · 2023Article
- Genome Editing and Diabetic Cardiomyopathy.Advances in experimental medicine and biology · 2023Article
- Low-Dose Empagliflozin Improves Systolic Heart Function after Myocardial Infarction in Rats: Regulation of MMP9, NHE1, and SERCA2a.International journal of molecular sciences · 2021Article
- Sustained Inhibition of NF-κB Activity Mitigates Retinal Vasculopathy in Diabetes.The American journal of pathology · 2021Article
- Network Pharmacology-Based Approach to Comparatively Predict the Active Ingredients and Molecular Targets of Compound Xueshuantong Capsule and Hexuemingmu Tablet in the Treatment of Proliferative Diabetic Retinopathy.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020Article
- The Peroxisome Proliferator-Activated Receptor-Gamma Coactivator-1α-Heme Oxygenase 1 Axis, a Powerful Antioxidative Pathway with Potential to Attenuate Diabetic Cardiomyopathy.Antioxidants & redox signaling · 2020Review
- MMP9 mediates acute hyperglycemia-induced human cardiac stem cell death by upregulating apoptosis and pyroptosis in vitro.Cell death & disease · 2020Article
- Electrical Stimulation of pediatric cardiac-derived c-kitStem cells (Dayton, Ohio) · 2019Article
- TFAM overexpression reduces pathological cardiac remodeling.Molecular and cellular biochemistry · 2019Article
- Targeting miRNA for Therapy of Juvenile and Adult Diabetic Cardiomyopathy.Advances in experimental medicine and biology · 2018Article
- Article
- Cardiac transcriptome profiling of diabetic Akita mice using microarray and next generation sequencing.PloS one · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Elevated expression and activity of matrix metalloproteinase-9 (MMP9) and decreased contractility of cardiomyocytes are documented in diabetic hearts. However, it is unclear whether MMP is involved in the regulation of contractility of cardiomyocytes in diabetic hearts. In the present study, we tested the hypothesis that MMP9 regulates contractility of cardiomyocytes in diabetic hearts, and ablation of MMP9 prevents impaired contractility of cardiomyocytes in diabetic hearts. To determine the specific role of MMP9 in cardiomyocyte contractility, we used 12-14 week male WT (normoglycemic sibling of Akita), Akita, and Ins(2+∕-)/MMP9(-∕-) (DKO) mice. DKO mice were generated by cross-breeding male Ins2(+∕-) Akita (T1D) with female MMP9 knockout (MMP9(-∕-)) mice. We isolated cardiomyocytes from the heart of the above three groups of mice and measured their contractility and calcium transients. Moreover, we determined mRNA and protein levels of sarco-endoplasmic reticulum calcium ATPase-2a (SERCA-2a), which is involved in calcium handling during contractility of cardiomyocytes in WT, Akita, and DKO hearts using QPCR, Western blotting and immunoprecipitation, respectively. Our results revealed that in Akita hearts where increased expression and activity of MMP9 is reported, the rates of shortening and re-lengthening (±dL/dt) of cardiomyocytes were decreased, time to 90% peak height and baseline during contractility was increased, rate of calcium decay was increased, and calcium transient was decreased as compared to WT cardiomyocytes. However, these changes in Akita were blunted in DKO cardiomyocytes. The molecular analyses of SERCA-2a in the hearts showed that it was downregulated in Akita as compared to WT but was comparatively upregulated in DKO. These results suggest that abrogation of MMP9 gene prevents contractility of cardiomyocytes, possibly by increasing SERCA-2a and calcium transients. We conclude that MMP9 plays a crucial role in the regulation of contractility of cardiomyocytes in diabetic hearts.
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