rno-mir-16: G Protein-Coupled Receptor Kinase 2 (Grk2) was identified as a potential target of rno-miR-15a and rno-mir-16, and downregulation of these miRNAs reduced thermal hyperalgesia and mechanical allodynia in rats with chronic constriction injury (CCI) [PMC8914318]. The expression of rno-miR-15a and rno-mir-16 was significantly increased in the spinal cord of CCI rats, suggesting their involvement in the development of neuropathic pain [PMC8914318]. Inhibition of rno-miR-15a and rno-mir-16 led to a remarkable increase in the expression of Grk2 in CCI rats [PMC8914318]. The miRNA transcripts observed in the blood and brain at 24 hours following reperfusion included rno-mir-16, -23a, -191, -292-5p, -320, -451, -494, and let-7. At 48 hours post-reperfusion, miRNAs such as miR-26a, -26b, -103, -107,-150,-185,-195,-191,-214,-320,-328,-352,-494,and let7 were observed [PMC4991681]. Rno-mir-16 was included as a control oligo for microarray analysis [PMC1790902]. Rno-mir-16 was reported to be involved in selenium deficiency-induced heart failure [PMC5920094]. In diabetic GK rats compared to Wistar and GK+Sita groups with lower expression levels of these microRNAs (rno-mir-16 included), several microRNAs were significantly upregulated [PMC5473486]. Rno-mir-16 was found to be common to both blood and brain at 24-hour reperfusion [PMC3606790]. Rno-mir-16 was identified as a putative binding site for miR-15b and miR-16 in the 3'UTR of Faim, suggesting Faim as a potential target for these miRNAs [PMC4508667]. Rno-mir-16 was among the muscle-specific circulating miRNAs associated with interstitial fibrosis, insulin resistance, and inflammation [PMC7667132]. Rno-mir-16 was exclusively expressed in the 24-hour samples [PMC8567963]. Several miRNAs, including rno-mir-16, were found to be associated with heart failure with preserved ejection fraction (HFpEF) development [PMC7667132].