MilliporeSigma
  • Home
  • Search Results
  • The sinus venosus contributes to coronary vasculature through VEGFC-stimulated angiogenesis.

The sinus venosus contributes to coronary vasculature through VEGFC-stimulated angiogenesis.

Development (Cambridge, England) (2014-11-08)
Heidi I Chen, Bikram Sharma, Brynn N Akerberg, Harri J Numi, Riikka Kivelä, Pipsa Saharinen, Haig Aghajanian, Andrew S McKay, Patrick E Bogard, Andrew H Chang, Andrew H Jacobs, Jonathan A Epstein, Kryn Stankunas, Kari Alitalo, Kristy Red-Horse
ABSTRACT

Identifying coronary artery progenitors and their developmental pathways could inspire novel regenerative treatments for heart disease. Multiple sources of coronary vessels have been proposed, including the sinus venosus (SV), endocardium and proepicardium, but their relative contributions to the coronary circulation and the molecular mechanisms regulating their development are poorly understood. We created an ApjCreER mouse line as a lineage-tracing tool to map SV-derived vessels onto the heart and compared the resulting lineage pattern with endocardial and proepicardial contributions to the coronary circulation. The data showed a striking compartmentalization to coronary development. ApjCreER-traced vessels contributed to a large number of arteries, capillaries and veins on the dorsal and lateral sides of the heart. By contrast, untraced vessels predominated in the midline of the ventral aspect and ventricular septum, which are vessel populations primarily derived from the endocardium. The proepicardium gave rise to a smaller fraction of vessels spaced relatively uniformly throughout the ventricular walls. Dorsal (SV-derived) and ventral (endocardial-derived) coronary vessels developed in response to different growth signals. The absence of VEGFC, which is expressed in the epicardium, dramatically inhibited dorsal and lateral coronary growth but left vessels on the ventral side unaffected. We propose that complementary SV-derived and endocardial-derived migratory routes unite to form the coronary vasculature and that the former requires VEGFC, revealing its role as a tissue-specific mediator of blood endothelial development.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Fibronectin human plasma, liquid, 0.1% (Solution), BioReagent, suitable for cell culture
Trolamine, European Pharmacopoeia (EP) Reference Standard
Sigma-Aldrich
Acetic anhydride, puriss. p.a., ACS reagent, reag. ISO, reag. Ph. Eur., ≥99% (GC)
Sigma-Aldrich
Acetic anhydride, ReagentPlus®, ≥99%
Sigma-Aldrich
Triethanolamine, reagent grade, 98%
Sigma-Aldrich
Acetic anhydride, 99.5%
Supelco
Acetic anhydride, for GC derivatization, LiChropur, ≥99.0%
Sigma-Aldrich
Triethanolamine, BioUltra, ≥99.5% (GC)
Sigma-Aldrich
Triethanolamine, puriss. p.a., ≥99% (GC)
Sigma-Aldrich
Triethanolamine, ≥99.0% (GC)
Sigma-Aldrich
Acetic anhydride, Arxada quality, ≥99.5% (GC)
Sigma-Aldrich
Acetic anhydride, ACS reagent, ≥98.0%
SAFC
Triethanolamine
Supelco
Triethanolamine, analytical standard
Sigma-Aldrich
Acetic anhydride