CD206+ macrophage is an accelerator of endometriotic-like lesion via promoting angiogenesis in the endometriosis mouse model

In endometriosis, M2 MΦs are dominant in endometriotic lesions, but the actual role of M2 MΦ is unclear. CD206 positive (+) MΦ is classified in one of M2 type MΦs and are known to produce cytokines and chemokines. In the present study, we used CD206 diphtheria toxin receptor mice, which enable to deplete CD206+ cells with diphtheria toxin (DT) in an endometriosis mouse model. The depletion of CD206+ MΦ decreased the total weight of endometriotic-like lesions significantly (p < 0.05). In the endometriotic-like lesions in the DT group, a lower proliferation of endometriotic cells and the decrease of angiogenesis were observed. In the lesions, the mRNA levels of VEGFA and TGFβ1, angiogenic factors, in the DT group significantly decreased to approximately 50% and 30% of control, respectively. Immunohistochemical study revealed the expressions of VEGFA and an endothelial cell marker CD31 in lesions of the DT group, were dim compared to those in control. Also, the number of TGFβ1 expressing MΦ was significantly reduced compared to control. These data suggest that CD206+ MΦ promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions.

Human muscle-derived CLEC14A-positive cells regenerate muscle independent of PAX7

Skeletal muscle stem cells, called satellite cells and defined by the transcription factor PAX7, are responsible for postnatal muscle growth, homeostasis and regeneration. Attempts to utilize the regenerative potential of muscle stem cells for therapeutic purposes so far failed. We previously established the existence of human PAX7-positive cell colonies with high regenerative potential. We now identified PAX7-negative human muscle-derived cell colonies also positive for the myogenic markers desmin and MYF5. These include cells from a patient with a homozygous PAX7 c.86-1G > A mutation (PAX7null). Single cell and bulk transcriptome analysis show high intra- and inter-donor heterogeneity and reveal the endothelial cell marker CLEC14A to be highly expressed in PAX7null cells. All PAX7-negative cell populations, including PAX7null, form myofibers after transplantation into mice, and regenerate muscle after reinjury. Transplanted PAX7neg cells repopulate the satellite cell niche where they re-express PAX7, or, strikingly, CLEC14A. In conclusion, transplanted human cells do not depend on PAX7 for muscle regeneration.

Possible involvement of pericytes in intraplaque hemorrhage of carotid artery stenosis

OBJECTIVEIntraplaque hemorrhage (IPH) is most often caused by the rupture of neovessels; however, the factors of intraplaque neovessel vulnerability remain unclear. In this study, the authors focused on pericytes and aimed to investigate the relationship between IPH and pericytes.METHODSThe authors retrospectively analyzed the medical records of all patients with carotid artery stenoses who had undergone carotid endarterectomy at their hospitals between August 2008 and March 2016. Patients with carotid plaques that could be evaluated histopathologically were eligible for study inclusion. Intraplaque hemorrhage was analyzed using glycophorin A staining, and patients were divided into the following 2 groups based on the extent of granular staining: high IPH (positive staining area > 10%) and low IPH (positive staining area ≤ 10%). In addition, intraplaque neovessels were immunohistochemically evaluated using antibodies to CD34 as an endothelial cell marker or antibodies to NG2 and CD146 as pericyte markers. The relationship between IPH and pathology for intraplaque neovessels was investigated.RESULTSSeventy of 126 consecutive carotid stenoses were excluded due to the lack of a specimen for histopathological evaluation; therefore, 53 patients with 56 carotid artery stenoses were eligible for study inclusion. Among the 56 stenoses, 37 lesions had high IPH and 19 had low IPH. The number of CD34-positive neovessels was equivalent between the two groups. However, the densities of NG2- and CD146-positive neovessels were significantly lower in the high IPH group than in the low IPH group (5.7 ± 0.5 vs. 17.1 ± 2.4, p < 0.0001; 6.6 ± 0.8 vs. 18.4 ± 2.5, p < 0.0001, respectively).CONCLUSIONSPlaques with high IPH are associated with fewer pericytes in the intraplaque neovessels. This finding may help in the development of novel therapeutic strategies targeting pericytes.

Immunohistochemical evaluation of neoangiogenesis in canine mast cell tumours

The aim of the study was to assess the microvessel density based on the analysis of the expression of the CD31, VEGF, and LIMS-1 proteins in canine mast cell tumours. The study was conducted on 60 mastocytomas; 16 cases were classified as the grade I, 26 as the grade II, and 18 as the grade III. Statistical analysis showed a positive correlation only between the grade of the tumour and the expression of LIMS-1. In conclusion, LIMS-1 could be successfully used as a prognostic endothelial cell marker in mast cell tumour. CD31 may be a useful marker, but further examinations are necessary. VEGF is not recommended

A Rare Presentation of Retiform Hemangioendothelioma in the External Auditory Canal

Retiform hemangioendothelioma is a rare intermediate or borderline neoplasm of the blood vessels that mostly occurs in extremities. Here we report a unique case of retiform hemangioendothelioma presented in the external auditory canal. 58-year-old male patient presented with the complaint of right ear swelling for 4 years. On examination, a spherical swelling in the right ear was found occluding the view of external auditory canal. The tumor was removed surgically. Intraoperatively, the mass was found attached to the outer part of the right external auditory canal near the root of helix. Histopathology of the resected tumor showed typical features of retiform hemangioendothelioma. In addition, immunohistochemical analysis revealed that tumor was positive for endothelial cell marker CD34 and occasionally positive for cell proliferative marker Ki-67.