Low pericyte coverage of endometrial microvessels in heavy menstrual bleeding correlates with the microvessel expression of VEGF-A

Emil Andersson, Eva Zetterberg, Inger Vedin, Kjell Hultenby, Jan Palmblad, Miriam Mints
In: International Journal of Molecular Medicine · 2014 · vol. 35(2) , pp. 433–438 · doi:10.3892/ijmm.2014.2035 · PMID:25504455 · W2135344378
article OA: bronze CC0 ⤵ 7 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

Endometrial microvessels in heavy menstrual bleeding patients exhibit low pericyte coverage correlated with increased VEGF-A expression, suggesting a link to vessel fragility.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This paper investigated whether endometrial microvessels in women with idiopathic heavy menstrual bleeding of endometrial origin (HMB-E) are fragile due to low pericyte coverage, compared with healthy ovulating controls, using immunohistochemical staining for smooth muscle actin-α (SMAα) and image analysis of microvascular density. In 10 women with HMB-E and 17 controls, microvascular density was similar between groups, but the number of SMAα-positive (pericyte-covered) microvessels in the proliferative phase was significantly lower in HMB-E; additionally, pericyte coverage did not vary by menstrual phase in HMB-E whereas it decreased from proliferative to secretory in controls. A significant negative correlation was reported between VEGF-A–positive microvessels and pericyte-covered microvessels, and the endothelial cell layer was thicker in HMB-E; a limitation is the small sample size and reliance on pericyte identification via SMAα positivity. This paper is centrally about endometriosis and/or adenomyosis? It is not directly focused on either condition, but it relates to endometriosis and adenomyosis through its study of endometrial microvascular instability mechanisms involving VEGF-A and pericyte coverage that may overlap with vascular pathology in those diseases.

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Abstract

A prospective clinical study was carried out to investigate whether endometrial microvessels in patients with idiopathic heavy menstrual bleeding (HMB) of endometrial origin (HMB-E) are fragile due to low pericyte coverage. Idiopathic HMB-E is characterized by large endothelial cell gaps related to the microvascular overexpression of vascular endothelial growth factor (VEGF)-A and VEGF receptors 1-3. A total of 10 women with a normal menstrual cycle and a history of HMB of <5 years, and 17 healthy women with a normal menstrual cycle were recruited from the Karolinska University Hospital. Blood samples were obtained for hormone analysis and coagulation tests. Endometrial biopsies were collected in the proliferative or in the secretory phase. Pericyte coverage was assessed using immunohistochemical staining for smooth muscle actin-α (SMAα) and by image analysis (microvascular density) of endometrial biopsies from 10 patients with HMB-E and 17 healthy ovulating women (control subjects). Previously published data on endothelial cell gap size and the expression of VEGF receptors were used. Although microvascular density did not differ between the patients with HMB-E and the control subjects, the number of SMAα-positive microvessels in the proliferative phase was significantly (P=0.005) lower in the patients with HMB-E than in the control subjects. Moreover, the number of SMAα-positive microvessels in the control subjects was significantly fewer in the secretory (P=0.04) than in the proliferative phase, whereas this number did not differ among the patients with HMB-E regardless of phase. A significant negative correlation was observed between the number of VEGF-A-positive microvessels and microvessels with pericyte coverage (r=0.8; P=0.04). Finally, the endothelial cell layer was significantly thicker in the patients with HMB-E than in the control subjects. Thus, the upregulation of VEGF-A in idiopathic HMB-E is associated with a low pericyte coverage during the proliferative phase of intense angiogenesis, which may confer vessel fragility, possibly leading to excessive blood loss.

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