Investigation of the Distribution and Changes of VLDLR Subtype in Fibrotic Cardiac Muscles

Very low-density lipoprotein receptor (VLDLR) is the major receptor with which cells can uptake the triacylglycerol from blood. It is divided into two subtypes according to presence of O- linked sugar domain located in the VLDLR receptor immediately outside of the membrane. Type Ⅰ VLDLR contains the O-link domain, while type Ⅱhas no such domain. The type ⅠVLDLR are mainly found on the surface of human myocardial cells. The result of our quantitative polymerase chain reaction on the normal and fibrotic cardiac muscles showed that both subtypes and expression level of VLDLR on the myocardial cell surface did not vary significantly between the normal and the fibrotic cardiac muscles despite the presence of malfunction due to fibrosis. This finding suggests that fibrosis doesn't exert significant influence on the subtype and the expression of VLDLR on the sur- face of myocardial cells. Such inconsistence with the changes found in other fibrotic tissues is awaiting further studies.

Effect of Cerium on Cardiac Muscle of Rat and Guinea Pig

The effect of Ce3+ on cardiac muscle of rat and guinea pig was studied. In vitro, 0.05 mmol·L-1 solution of Ce3+ inhibited the contraction of guinea pig atria. The change of action potential duration(APD) of guinea pig papillary muscle exposed to 0.4 mmol·L-1 Ce3+ was significant, and those exposed to 0.1 and 0. 2 mmol·L-1 Ce3+ were not significant. In vivo, compared with the control group, the APD for rat cardiac muscle after long-term feed on Ce3+ was significantly delayed in high dose, and that was not significantly delayed in low dose. The results suggest that Ce3+ with long-term high dose intake might affect the influx of Ca2+, Na+ and outflow of K+ for rat cardiac muscle.

Effect of Hypoxia on Ca^(2+) Concentration in Broiler's Cardiac Muscle Cells

The purpose of this research was to study the effect of hypoxia on the Ca^2＋ concentration in broiler＇s cardiac muscle cells （CMCs）. The concentration of Ca^2＋ in the CMC was observed using a laser scanning confocal microscope （LSCM）. The results showed that hypoxia could significantly increase intracellular Ca^2＋（normal oxygen, 99.3 ＋_ 13.1; hypoxia, 129.4 ＋_ 24.3, P 〈 0.01） in CMCs. The Ca^2＋ antagonist （nifedipine, verapamil） could significantly restrain the Ca^2＋ influx across the cell membrane of CMC treated by hypoxia （CMC： hypoxia ＋ verapamil, 100.9± 28.2; hypoxia ＋ nifedipine, 107.6± 27.7; P 〈 0.01）. The results showed hypoxia could increase intracellular Ca^2＋ concentration of CMC, and the Ca^2＋ antagonist could restrain the Ca^2＋ influx across the cell membrane of CMC treated by hypoxia.

The Effect of Fructose-1,6-diphosphate and HTK Solution on Protecting Primary Cardiac Muscle Cells of Rat with Cold Preservation

In this study we tried to investigate the effect of fructose-1,6-diphosphate and HTK solution on protecting primary cardiac muscle cells of rat with cold preservation. The primary cardiac muscle cells of rat were cultured in vitro with four preservation solutions respectively: 0.9 % sodium chloride solution (group A), FDP (group B), HTK solution (group C) and a mixture of FDP and HTK solution (group D). The cells were preserved for 6, 8 and 10 h at 0-4 ℃. The values of AST and LDH-L and the Na+-K+ ATPase activity in cardiac muscle cells were detected, and the survival rate of cardiac muscle cells was detected with trypan blue staining. The values of AST and LDH-L in group C and group D were remarkable lower those in group A and group B (P<0.001), while the Na+-K+ ATPase activity and the survival rate of cells in group C and group D were much higher than those in group A and group B (P<0.001). The values of AST and LDH-L after 6 hours in group D decreased much more than those in group C (P<0.01), while the Na+-K+ ATPase activity and the survival rate of cells in group D improved more than those in group C (P<0.01). Both of the HTK solution and the mixture of HTK and FDP solution have an evident effect on protecting the primary cardiac muscle cells of rat in vitro with cold preservation, Compared with the HTK solution, the mixture solution has a better short-term protective effect.

Rbfox1 controls alternative splicing of focal adhesion genes in cardiac muscle cells

Alternative splicing is one of the major cellular processes that determine the tissue-specific expression of protein variants.However,it remains challenging to identify physiologically relevant and tissue-selective proteins that are generated by alternative splicing.Hence,we investigated the target spectrum of the splicing factor Rbfox1 in the cardiac muscle context in more detail.By using a combination of in silico target prediction and in-cell validation,we identified several focal adhesion proteins as alternative splicing targets of Rbfox1.We focused on the alternative splicing patterns of vinculin(metavinculin isoform)and paxillin(extended paxillin isoform)and identified both as potential Rbfox1 targets.Minigene analyses suggested that both isoforms are promoted by Rbfox1 due to binding in the introns.Focal adhesions play an important role in the cardiac muscle context,since they mainly influence cell shape,cytoskeletal organization,and cell–matrix association.Our data confirmed that depletion of Rbfox1 changed cardiomyoblast morphology,cytoskeletal organization,and multinuclearity after differentiation,which might be due to changes in alternative splicing of focal adhesion proteins.Hence,our results indicate that Rbfox1 promotes alternative splicing of focal adhesion genes in cardiac muscle cells,which might contribute to heart disease progression,where downregulation of Rbfox1 is frequently observed.

Smyd1 is essential for myosin expression and sarcomere organization in craniofacial,extraocular,and cardiac muscles

Skeletal and cardiac muscles are striated myofibers that contain highly organized sarcomeres for muscle contraction.Recent studies revealed that Smyd1,a lysine methyltransferase,plays a key role in sarcomere assembly in heart and trunk skeletal muscles.However,Smyd1 expression and function in craniofacial muscles are not known.Here,we analyze the developmental expression and function of two smyd1 paralogous genes,smyd1 a and smyd1 b,in craniofacial and cardiac muscles of zebrafish embryos.Our data show that loss of smyd1a(smyd1a^(mb5))or smyd1b(smyd1b^(sa15678))has no visible effects on myogenic commitment and expression of myod and myosin heavy-chain m RNA transcripts in craniofacial muscles.However,myosin heavy-chain protein accumulation and sarcomere organization are dramatically reduced in smyd1b^(sa15678) single mutant,and almost completely diminish in smyd1a^(mb5);smyd1b^(sa15678) double mutant,but not in smyd1a^(mb5) mutant.Similar defects are also observed in cardiac muscles of smyd1b^(sa15678) mutant.Defective craniofacial and cardiac muscle formation is associated with an upregulation of hsp90α1 and unc45b mRNA expression in smyd1b^(sa15678) and smyd1a^(mb5);smyd1b^(sa15678) mutants.Together,our studies indicate that Smyd1b,but not Smyd1a,plays a key role in myosin heavy-chain protein expression and sarcomere organization in craniofacial and cardiac muscles.Loss of smyd1b results in muscle-specific stress response.

Histopathological Evaluation of the Cardiotoxicity of Dihydroartemisinin-Piperaquine on Male Albino Rats

Problem Statement: Malaria’s global impact necessitates effective treatments, like dihydroartemisinin-piperaquine (DHA/PQP), though safety concerns, notably drug-induced cardiotoxicity (DICT), persist. A knowledge gap exists regarding DHA/PQP’s cardiac effects, warranting a comprehensive investigation. Approach: This study aimed to assess KROSH (DHA/PQP) impact on albino rat heart histology, examining structural changes and potential cardiotoxicity. 40 albino rats were grouped by KROSH dosage and duration, monitored for weight changes, and heart tissues were examined using hematoxylin and eosin (H & E) staining. Statistical analysis compared to control and treated groups. Results: KROSH administration led to varying rat weight effects, yet not statistically significant. Histological analysis revealed dose and duration-dependent cardiac tissue alterations, including distortion, adipose deposits, artery hypertrophy, fibrosis, and necrosis. These contrasts with prior research documenting DHA/PQP’s non-toxic effects. Conclusion/Recommendation: This study highlights potential KROSH (DHA/PQP) cardiotoxicity concerns through histological changes, underscoring the need for further research into underlying mechanisms and human health implications. Given DHA/PQP’s wide use, these findings should inform safety evaluations and administration practices.

The research of HSPB1 in apoptosis,autophagy and cardiogenic shock

Cardiogenic shock(CS)is a common cause of mortality and treatment remains challenging despite advances in therapeutic options.CS is caused by severe impairment of myocardial performance that results in decreased cardiac output,hypoperfusion of the end organ,and hypoxia.Clinically this presents as hypotension refractory to volume resuscitation with features of end-organ hypoperfusion requiring pharmacological or mechanical intervention.Acute myocardial infarction(AMI)accounts for 81%of patients with CS.Heat shock protein family B member 1(HSPB1)is a multifunctional protein induced by various stress factors and has a protective effect on cells.A large number of studies have demonstrated that HSPB1 plays an important role in regulating apoptosis.Recently,some studies have suggested that HSPB1 also participates in the autophagic process.HSPB1 are expressed in many cells of the cardiovascular system such as endothelial cells,cardiac muscle cells,monocytes,and platelets.They are up-regulated in response to inflammation,oxidative stress,or ischemia and protect cells against extracellular stress factors.Here,we explore the involvement of HSPB1 in apoptosis,autophagy,and CS.We speculate that HSPB1 may exert its anti-myocardial injury role via the regulation of apoptosis and autophagy;this may provide the basis for the development of new approaches for the prevention and treatment of CS.