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Cardiac Myosin Heart - Crossref

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Last Updated: 16 February 2022

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Abstract 17755: Cardiac Myosin Binding Protein C Contributes to the Protection of the Heart During Immune Response to Infection

Infections can exacerbate heart disease and contribute to heart transplant rejection. In comparison to WT hearts, MyBPC3 hearts have considerably fewer myeloid cells characterized by CD11b+GR1High in comparison to LPS hearts prior to the LPS challenge. In WT, the challenge to myeloid cell proliferation has dramatically raised myeloid cell count, but not in MyBPC3 hearts. B cells infiltration into MyBPC3 hearts only increased B cells, which means that B cells in B cells are correlated with increased cardiac myocyte cell death, which is consistent with increased cardiac myocyte cell death. In spleen and bone marrow, MyBPC3 showed decreased myeloid cell populations. These findings show that CD11b+GR1High cells are myeloid derived suppressor cells that shield cardiac myocytes during an immune response, and B cells are associated with cardiac myocyte cell death. These findings, in turn, show that modulating MDSC recruitment and MyBPC3 preservation may have the ability to treat heart failure and heart transplant rejection.

Source link: https://doi.org/10.1161/circ.130.suppl_2.17755


Abstract 17381: Cardiac Myosin I as a New Potential Biomarker for Prognosis of Acute Decompensated Heart Failure

Cardiac myosin I is one of a superfamily of motor proteins that is mostly present in myocardium. Several studies reported that serum CM-I levels in patients with acute coronary syndrome increased in patients with acute coronary syndrome. Patients with eight ACS patients and 22 patients with no reports of serum CM-I levels were excluded. As a prognostic survivor marker, we determined the difference in serum BNP levels between admission and discharge. According to the respective numbers, the number of patients with NYHA III and IV was between 30 and 36. Mean serum BNP and Troponin T were 934. 0 pg/ml and 0. 092 ng/ml, respectively, on admission, respectively. Serum CM-I levels showed a strong correlation with TrT levels and a poor relationship with BNP levels, which was not evident with BNP levels. CM-I levels were highly correlated with delta BNP, but TrT were not related to delta BNP. Conclusion: We discovered that CM-I was correlated with the difference in BNP between admission and discharge in ADHF patients.

Source link: https://doi.org/10.1161/circ.138.suppl_1.17381


Abstract 91: Pathogenicity of Naturally Produced Fragments of Cardiac Myosin Binding Protein C and Their Effects on Heart Function and Failure

Background: Myosin binding protein C is a thick filament protein made up of 1274 amino acid residues and mutations in the cardiac isoform, accounting for a significant number of reported cases of familial hypertrophic cardiomyopathy. Methods and Results: We wanted to determine the potential pathogenicity of the 40kd fragment in vivo, so we created cardiac myocyte-specific transgenic mice using a Tet-Off inducible system to encourage controlled expression in cardiomyocytes. When 40kD protein expression is stimulated by crossing the responder mice with tetracycline transactivator mice, the double TG mice develop protein expression, sarcomere dysgenesis, and altered cardiac geometry when responding to the responder mice are crossed. MEK-ERK hypertrophic signaling pathways were activated by subsequent analysis, resulting in the production of MEK-ERK hypertrophic signaling pathways. Conclusions: The findings reveal that a 40kD cMyBP-C fragment, which occurs during heart disease development in both mouse and human, is a pathogenic fragment whose presence causes hypertrophic cardiomyopathy and heart failure.

Source link: https://doi.org/10.1161/res.111.suppl_1.a91


Abstract 17263: Cardiac Myosin Binding Protein-C Phosphorylation Mitigates Pressure-Overload Heart Failure Despite Alterations in Calcium Handling

Heart failure with reduced ejection fractions exhibits both systolic and diastolic dysfunctions, and, as a result, systolic and diastolic dysfunctions; therefore, treatments that increase contractility and lusitropy can be very helpful. For all mouse models, serial echocardiography revealed that cardiac structure and function had deteriorated. T3SA demonstrated ventricular dilation and decreased ejection fraction in comparison to tWT at post-TAC week-5, reducing the ejection fraction in comparison to tWT, which was also reduced; conversely, t3SD displayed improved diastolic function preservation during diastolic function; tWT showed better retention of diastolic function compared to tWT at post-TAC week-5. Tubular calcium deposition accelerated by electrically paced intact papillary muscles from t3SA and t3SD, which revealed slower intracellular calcium deposition. Lower calcium phosphate expression in t3SA and t3SD, the lowest ryanodine receptor expression in t3SD, and reduced calcium phosphate reduction in t3SD was only evident in t3SD, according to western blotting, with lower calcium phosphate reduction in t3SD and t3SD.

Source link: https://doi.org/10.1161/circ.132.suppl_3.17263

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

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* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions