| First Author | Mouat MA | Year | 2021 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 321 |
| Issue | 4 | Pages | H807-H817 |
| PubMed ID | 34533400 | Mgi Jnum | J:310474 |
| Mgi Id | MGI:6762448 | Doi | 10.1152/ajpheart.00198.2021 |
| Citation | Mouat MA, et al. (2021) Involvement of GPR37L1 in murine blood pressure regulation and human cardiac disease pathophysiology. Am J Physiol Heart Circ Physiol |
| abstractText | Multiple mouse lines lacking the orphan G protein-coupled receptor, GPR37L1, have elicited disparate cardiovascular phenotypes. The first published Gpr37l1 knockout mice study (1) indicated a marked elevation in systolic blood pressure (SBP; ~60 mmHg), revealing a potential therapeutic opportunity. The phenotype differs from our independently generated knockout line, where male mice exhibited equivalent baseline blood pressure to wildtype (2, 3). Here, we attempted to reproduce the findings of Min et al. (1) by characterizing the cardiovascular phenotype of both the original knockout and transgenic lines alongside a C57BL/6J control line, using the same method of blood pressure measurement. The present study supports the findings from our independently developed Gpr37l1 knockout line (2, 3), namely that SBP and diastolic blood pressure (DBP) are not different in the original Gpr37l1 knockout male mice (SBP: 130.9+/-5.3 mmHg; DBP: 90.7+/-3.0 mmHg) compared to C57BL/6J mice (SBP: 123.1+/-4.1 mmHg; DBP: 87.0+/-2.7 mmHg) (2, 3). Instead, we attribute the apparent hypertension of the knockout line described by Min et al. (1) to comparison with a seemingly hypotensive transgenic line (SBP 103.7+/-5.0 mmHg; DBP 71.9+/-3.7 mmHg). Additionally, we quantified myocardial GPR37L1 transcript in humans, which was suggested to be downregulated in cardiovascular disease (1). We found that GPR37L1 has very low native transcript levels in human myocardium, and that expression is not different in tissue samples from patients with heart failure compared to gender-matched healthy control tissue. These findings indicate that cardiac GPR37L1 expression is unlikely to contribute to the pathophysiology of human heart failure. |
