Transcriptional abundance and cyto-protective action of class I small heat shock proteins in heat stressed caprine cardiac cells

The present study was aimed to document the transcriptional abundance and cyto-protective action of class I small heat shock proteins (HSPs) in heat stressed caprine cardiac cells. Cardiac cells were isolated from different heart tissues (n = 6) of goats and primary cardiac cells culture was done. Primary cardiac cells achieved 75–80 % confluence after 72 h of incubation. Further, confluent cardiac cells were exposed to heat stress at 42 °C for 0 (control), 20, 60, 100 and 200 min. Transcriptional abundance of HSPB1 did not change at 20 min, up-regulated (P < 0.05) from 60 to 200 min and registered highest at 200 min of heat stress. Transcriptional abundance of HSPB5 and HSPB8 did not vary at 20 and 60 min and then significantly increased at 100 and 200 min with highest transcription at 200 min of heat stress. Transcriptional abundance of HSPB6 was elevated only at 200 min of heat stress. Transcriptional abundance of Caspase-3 was significantly decreased at 200 min of heat stress. Therefore, it is logical to speculate that differential transcriptional abundance of class I small HSPs at different durations of heat stress might maintain cardiac cell homeostasis during heat stress. Moreover, highest transcription of class I small HSPs might have down-regulated the transcriptional abundance of Caspase-3 at 200 min of heat stress suggesting their cyto-protective action on heat stressed caprine cardiac cells. • Transcriptional abundance of class I small HSPs was found to be highest following 200 minutes of heat stress at 42 °C in caprine cardiac cells. • Amongst class I small HSPs, HSPB1 may be a potential biomarker to quantify the intensity of heat stress in caprine cardiac cells. • Transcriptional abundance of Caspase-3 was found to be lowest following 200 minutes of heat stress at 42 °C in caprine cardiac cells. • Differential transcription of class I small HSPs at different durations of heat stress might maintain cardiac cell homeostasis during heat stress.