The regulation of p42/p44 mitogen-activated protein kinases in the injured rat carotid artery
Research article published in Journal of surgical research (1997)
Abstract
UNLABELLED: Arterial smooth muscle cell (SMC) proliferation is an important factor in the development of atherosclerotic plaques and restenotic lesions following arterial reconstruction. Basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), and thrombin are known to induce SMC proliferation and migration in vitro and in vivo. In cultured cells the proliferative responses to these mitogens depend on the activation of the p42/p44 mitogen-activated protein kinases (MAPKs), whereas the role of these kinases in vivo has yet to be established. We tested whether MAPK activity is induced following vessel injury and whether activity is dependent on the release of bFGF, PDGF, and thrombin. Following balloon injury of the left carotid of male Sprague-Dawley rats, arteries were removed and analyzed with respect to MAPK activity, BrdU-labeled nuclei, and/or luminal, medial, and intimal areas. MAPK activity is induced in the rat carotid artery following balloon-catheter injury with a maximum activation at 30 min with a return to just above baseline at 11 hr after injury. Intravenous administration of heparin or neutralizing antibodies to bFGF or PDGF prior to injury reduced SMC proliferation and neointimal lesional formation but did not affect the early induction of MAPK activity. Administration of a tissue factor inhibitor or thrombin inhibitor also did not affect MAPK activity, although it impaired the initiation of the coagulation cascade. IN CONCLUSION: (1) MAPK is activated in a time-dependent manner in response to injury; (2) the antiproliferative effect of heparin in vivo is not mediated through the inhibition of MAPK activity induced 30 min after injury; (3) the activation of MAPK after 30 min is not dependent on PDGF, bFGF, or thrombin following vessel injury in the rat.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
The regulation of p42/p44 mitogen-activated protein kinases in the injured rat carotid artery.
Por qué esto importa para la hirudoterapia
This study investigated the activation of p42/p44 mitogen-activated protein kinases (MAPKs) in rat carotid arteries following balloon-catheter injury, evaluating whether this activation depends on thrombin, basic fibroblast growth factor, or platelet-derived growth factor. Researchers found that while heparin and neutralizing antibodies reduced smooth muscle cell proliferation, early MAPK activation was not dependent on thrombin or the other tested factors. While it touches on vascular hemostatic pathways that fall under the broader ASH domain, the provided abstract contains absolutely no mention of leeches, hirudin, or hirudotherapy. Therefore, based strictly on the provided text, the relevance to leech therapy or the leech secretome is entirely absent.
Citación
The regulation of p42/p44 mitogen-activated protein kinases in the injured rat carotid artery
Lille ST et al. · Journal of surgical research, 1997
Contexto clínico relacionado
Explore cómo esta investigación se conecta con la práctica clínica
Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: June 18, 2026