Endometriosis and cancer have much in common, notably their burgeoning of cells in hypoxic milieus, their invasiveness, and their capacity to trigger remodeling, vascularization, and innervation of other tissues. An important role in these processes is played by permissive microenvironments inhabited by a variety of stromal and immune cells, including macrophages. Remarkable phenotypical plasticity of macrophages makes them a promising therapeutic target; some key issues are the range of macrophage phenotypes characteristic of a particular pathology and the possible manners of its modulation. In both endometriosis and cancer, macrophages guard the lesions from immune surveillance while promoting pathological cell growth, invasion, and metastasis. This review article focuses on a comparative analysis of macrophage behaviors in endometriosis and cancer. We also highlight recent reports on the experimental modulation of macrophage phenotypes in preclinical models of endometriosis and cancer.
Background: Macrophages play a key role in liver regeneration. The fates of resident macrophages after 70% resection are poorly investigated. In this work, using the MARCO macrophage marker (abbreviated from macrophage receptor with collagenous structure), we studied the dynamics of mouse liver resident macrophages after 70% resection. Methods: In BALB/c male mice, a model of liver regeneration after 70% resection was reproduced. The dynamics of markers CD68, TIM4, and MARCO were studied immunohistochemically and by using a Western blot. Results: The number of MARCO- and CD68-positive macrophages in the regenerating liver increased 1 day and 3 days after resection, respectively. At the same time, the content of the MARCO protein increased in the sorted macrophages of the regenerating liver on the third day. Conclusions: The data indicate that the number of MARCO-positive macrophages in the regenerating liver increases due to the activation of MARCO synthesis in the liver macrophages. The increased expression of MARCO by macrophages can be regarded as a sign of their activation. In the present study, stimulation with LPS led to an increase in the expression of the Marco gene in both Kupffer cells and macrophages of bone marrow origin.
The aim of this study was to evaluate the efficacy of hysteroscopically controlled injections of autologous platelet-rich plasma (PRP) and autologous endometrial cells as a treatment for infertile women with thin endometrium. The study enrolled 115 patients with thin endometrium (< 7 mm at implantation window) and infertility, who were divided into groups: Group 1 (the control) underwent conservative therapy; Group 2 received intraendometrial PRP injections instead of the conservative therapy; Group 3 received identical injections after conservative therapy; Group 4 received injections of the autologous endometrial cells suspended in PRP. A single injection dose of PRP contained 0.6–0.7 × 1011 of platelets. The levels of PDGF-BB and VEGF in PRP were increased compared with ordinary plasma. The autologous endometrial cells, obtained from pipelle biopsies, constituted heterogeneous cell populations containing stromal and epithelial cells. Intraendometrial PRP injections had significant impact on endometrial thickness and local microcirculation in Group 2 and Group 3. In Group 4, injections of PRP reinforced with endometrial cells also facilitated a significant increase in endometrial thickness. This work describes a novel approach for infertility treatment in patients with refractory thin endometrium. PRP injections and injections of the endometrial cells suspended in PRP into endometrium enhanced cell proliferation and angiogenesis.
Background Platelet-rich plasma (PRP), which represents a valuable source of growth factors, is increasingly being applied in regenerative medicine. Recent findings suggest the feasibility of using PRP in the treatment of infertility secondary to refractory thin endometrium. Mesenchymal stem/stromal cells (MSCs) of the endometrium are an essential cellular component responsible for extracellular matrix remodeling, angiogenesis, cell-to-cell communication, and postmenstrual tissue repair. Using a rat model, we examine the effects of autologous PRP on MSCs isolated from the uterus and compare them with the effects of autologous ordinary plasma (OP) and complete growth medium. Methods MSCs were isolated from uterine tissues via enzymatic disaggregation. Flow cytometry immunophenotyping of the primary cell cultures was complemented by immunocytochemistry for Ki-67 and vimentin. The ability of MSCs to differentiate in osteo-, chondro-, and adipogenic directions was assessed using differentiation-inducing media. The levels of autophagy and apoptosis markers, as well as the levels of matrix metalloproteinase 9 (MMP9) and estrogen receptor α, were assessed by western blotting. Results After 24 h incubation, the proliferation index of the PRP-treated MSC cultures was significantly higher than that of the MSC cultures treated with complete growth medium. PRP treatment elevated production of LC3B protein, an autophagy marker, while OP treatment upregulated the expression of stress-induced protein p53 and extracellular enzyme MMP9. The results indicate practical relevance and validity for PRP use in the treatment of infertility.
Endometriosis is an estrogen‐dependent chronic inflammatory disease characterized by the presence of endometrial stroma and glands outside the endometrium. The gold standard in the treatment of endometriosis is laparoscopy but after that, the relapse rate is about 50%. Thus, the search for new effective non‐invasive methods of endometriosis therapy is an actual problem. Endometriosis has many properties similar to tumors including the fact that macrophages with an anti‐inflammatory phenotype (M2) prevail in the foci of endometriosis. It is already known that activated macrophages with a pro‐inflammatory phenotype (M1) have an antitumor effect. In this regard, we hypothesized that increasing the proportion of M1 macrophages could help in the treatment of endometriosis. The objectives of our work were (1) to assess the expression profile of macrophages in the foci of endometriosis in mice model of endometriosis; (2) to test the efficacy of administration of reprogrammed M1 macrophages as a possible anti‐endometrioid agent in the mouse. We studied the phenotypic profile of macrophages in the foci of endometriosis and the anti‐endometrioid activity of M1 macrophages on in vivoallogeneic model of mouse endometriosis induced in ovariectomized mice after intraperitoneal transplantation of the mouse uterus accompanied by 17β‐estradiol therapy. Analysis of the phenotypic profile of macrophages in the foci of endometriosis was carried out using immunohistochemical staining, western blot analysis, and qPCR. We obtained a reproducible model with lesions that had characteristic morphology. It was shown that macrophages with an anti‐inflammatory arginase1+ phenotype prevail in the foci of endometriosis compared with the intact endometrium. After verifying endometriosis development in mice, the experimental group was injected with M1‐polarized macrophages, while the control group was injected with unpolarized macrophages, and then the animals were monitored for two weeks. Macrophage cell line RAW264 was incubated with lipopolysaccharide (100 ng/ml) for 24 h to obtain M1‐polarized macrophages. M1‐polarization was verified by significant up‐regulation of MARCO, iNOS markers using western blot and qPCR analysis. After treatment of animals with M1 macrophages, we found that the number of foci and their sizes significantly decreased (p<0.05) in comparison with control animals. In our work, we proved the predominance of anti‐inflammatory macrophages in the foci of endometriosis and obtained the first results of a positive effect of M1 macrophages on the regression of foci of endometriosis.
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