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Angiotensin II causes cellular proliferation in infantile haemangioma via angiotensin II receptor 2 activation
  1. Tinte Itinteang1,
  2. Reginald Marsh1,
  3. Paul Frank Davis1,
  4. Swee Thong Tan1,2
  1. 1Gillies McIndoe Research Institute, Wellington, New Zealand
  2. 2Centre for the Study & Treatment of Vascular Birthmarks, Wellington Regional Plastic Maxillofacial and Burns Unit, Hutt Hospital, Wellington, New Zealand
  1. Correspondence to Dr Swee T Tan, Gillies McIndoe Research Institute, PO Box 7184, Newtown Wellington 6242, New Zealand; swee.tan{at}gmri.org.nz

Abstract

Aims To investigate the effect of the angiotensin peptides and their agonists and antagonists on cellular proliferation in proliferating infantile haemangioma (IH) in vitro explants.

Methods Proliferating IH samples from six patients were cultured in vitro in the presence of angiotensin I (ATI) alone, or AT1 and the ACE inhibitor, ramipril, or ATII alone, or ATII with the ATII receptor 1 (ATIIR1) blocker, losartan, or ATII with the ATIIR2 blocker, PD123319, or the ATIIR2 agonist, CGP42112. After 6 days in culture, the IH tissue pieces were harvested, formalin-fixed and paraffin-embedded. The effect of each treatment type on cellular proliferation was evaluated by immunohistochemical staining of these tissue pieces using the proliferation marker, Ki67.

Results There was a significant increase in cellular proliferation in the ATI and ATII treated IH tissues compared with control samples. Their effect on cellular proliferation was reduced by adding ramipril and PD123319, respectively. CGP42112, but not losartan, significantly increased cellular proliferation.

Conclusions Our findings suggest a key regulatory role of ATI and ATII in promoting cellular proliferation in IH, and establish a role for ACE and ATIIR2 in the proliferation of this tumour.

  • HISTOPATHOLOGY
  • IMMUNOCYTOCHEMISTRY
  • KI 67

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