@entity5175 induces distinct cell XXXX mechanisms in H9C2 cells and its differentiated form.

@entity1 @entity5175 @entity296 @entity796 @entity384 @entity2348 @entity281 @entity1167 @entity204 @entity2401
@entity2348 in myocardium may lead to the @entity296 , which may progress to @entity384 and @entity1167 . @entity796 has been reported to cause @entity2401 and other @entity281 especially in immunocompromised @entity1 . To understand the cellular responses during the establishment of @entity281 in myocardium, we challenged differentiated H9C2 cells with @entity5175 . We also did comparison studies with infected undifferentiated form of H9C2 cells. Invasion studies revealed that @entity5175 can invade both forms of cells and is able to survive and replicate within the host. Internalization of @entity5175 was confirmed by live cell imaging and flow cytometry analysis. Though invasion of the pathogen triggered an increased ROS production in the host cells at earlier post- @entity281 periods, it was decreased at later post- @entity281 periods. Invasion of @entity5175 induced cell @entity204 through apoptosis in differentiated H9C2 cells. Significant decrease in cell size, formation of polarized mitochondria, and nuclear fragmentation were observed in the infected differentiated cells. On the contrary, cell @entity204 preceded by multinucleation was observed in infected undifferentiated H9C2 cells. Morphological markers such as multinuclei and micro nuclei were observed. Cell cycle arrest in G2/M phase corroborates that the undifferentiated H9C2 cells experienced cell @entity204 preceded by multinucleation.
