Regulatory proteins in placental angiogenesis

The vasculature of the placenta plays a crucial role during the course of pregnancy in order to maintain the growing need of the fetus. Abnormal placental structure and function significantly increase the risk of stillbirth. Various growth factors and cytokines play an important role in the vasculogenesis and angiogenesis of placenta. These processes are stimulated by various pro-angiogenic factors. The activities of these factors are also stimulated by hypoxia. In some of the physiological phenomenon like ovulation, embryogenesis as well as in wound healing intense blood vessel growth can be seen similar to that seen in placenta. Therefore, factors that induce and maintain placental vascular growth and function are of considerable developmental and clinical significance. The total arterial architecture may also depend upon the pro-angiogenic factors. Hormones and other growth factors are other contributors of this vasculogenesis and angiogenesis. Any dysfunction of factors can lead to foetal hypoxia and related complications. This review describes the major growth factors and their significant role in vasculogenesis and angiogenesis of placenta.

Updates on Anticancer Therapy-Mediated Vascular Toxicity and New Horizons in Therapeutic Strategies

Vascular toxicity is a frequent adverse effect of current anticancer chemotherapies and often results from endothelial dysfunction. Vascular endothelial growth factor inhibitors (VEGFi), anthracyclines, plant alkaloids, alkylating agents, antimetabolites, and radiation therapy evoke vascular toxicity. These anticancer treatments not only affect tumor vascularization in a beneficial manner, they also damage ECs in the heart. Cardiac ECs have a vital role in cardiovascular functions including hemostasis, inflammatory and coagulation responses, vasculogenesis, and angiogenesis. EC damage can be resulted from capturing angiogenic factors, inhibiting EC proliferation, survival and signal transduction, or altering vascular tone. EC dysfunction accounts for the pathogenesis of myocardial infarction, atherothrombosis, microangiopathies, and hypertension. In this review, we provide a comprehensive overview of the effects of chemotherapeutic agents on vascular toxicity leading to hypertension, microvascular rarefaction thrombosis and atherosclerosis, and affecting drug delivery. We also describe the potential therapeutic approaches such as vascular endothelial growth factor (VEGF)-B and prokineticin receptor-1 agonists to maintain endothelial function during or following treatments with chemotherapeutic agents, without affecting anti-tumor effectiveness.

Klippel Trenaunay Syndrome: A Brief Overview

Klippel-Trenaunay syndrome is a rare congenital vascular disease. The pathogenesis of this syndrome is unclear, but it is thought that most cases are the result of somatic mutations that affect genes that play a role in vasculogenesis and angiogenesis. Some patients come with a triad of capillary malformation (hemangioma or port-wine stain), venous varicosities and bony or soft tissue hypertrophy. Clinical presentation of this syndrome can lead to significant morbidities and mortalities due to severe bleeding and emboli. Although the number of cases is low, a doctor must be able to distinguish Klippel-Trenaunay Syndrome from other rare vascular disorders. Parkes Weber syndrome is usually similar to Klippel-Trenaunay syndrome, except in the arterial malformations associated with capillary malformations and soft tissue to skeletal or bone hypertrophy. The diagnosis of Klippel-Trenaunay Syndrome is carried out clinically and is quite difficult to do even with experienced doctors because there is no precise pathognomonic test. There are several options in relation to the management of Klippel-Trenaunay Syndrome and non-invasive procedure is considered to be the most important of therapy modalities. Early diagnoses, progression monitoring, and proper intervention should be carried out for better prognosis and preventing complication.

Klippel Trenaunay Syndrome: A Brief Overview

A B S T R A C TKlippel-Trenaunay syndrome is a rare congenital vascular disease. The pathogenesisof this syndrome is unclear, but it is thought that most cases are the result of somaticmutations that affect genes that play a role in vasculogenesis and angiogenesis. Somepatients come with a triad of capillary malformation (hemangioma or port-wine stain),venous varicosities and bony or soft tissue hypertrophy. Clinical presentation of thissyndrome can lead to significant morbidities and mortalities due to severe bleedingand emboli. Although the number of cases is low, a doctor must be able to distinguishKlippel-Trenaunay Syndrome from other rare vascular disorders. Parkes Webersyndrome is usually similar to Klippel-Trenaunay syndrome, except in the arterialmalformations associated with capillary malformations and soft tissue to skeletal orbone hypertrophy. The diagnosis of Klippel-Trenaunay Syndrome is carried outclinically and is quite difficult to do even with experienced doctors because there is noprecise pathognomonic test. There are several options in relation to the managementof Klippel-Trenaunay Syndrome and non-invasive procedure is considered to be themost important of therapy modalities. Early diagnoses, progression monitoring, andproper intervention should be carried out for better prognosis and preventingcomplication.

Placental vasculogenesis and angiogenesis in women undergoing chemotherapy

Aim: to study placental vasculogenesis and angiogenesis in women receiving chemotherapy. Patients and Methods: placental structure was examined in 57 pregnant women aged 22–38 years who were subdivided into 3 groups, i.e., women with malignancies receiving or not receiving chemotherapy and healthy controls. The slices of the central part of placentas collected after childbirth were examined. Immunohistochemistry (IHC) was performed after standard histology. IHC intensity was assessed for CD31 and CD34. In addition to IHC intensity, the number of positive cells per field of view was calculated for VEGF, VEGFR1, and VEGFR2. Mean counts of positive cells separately for epithelial and stromal cells were calculated for eNOS. Results: in the control group, the maturity of the placental villous tree matched the gestational age. Meanwhile, in 100% of pregnant women with malignancies receiving chemotherapy and in 46.8% of pregnant women with malignancies not receiving chemotherapy, the maturity of the placental villous tree was 2–4 weeks behind the gestational age. IHC revealed no significant differences in the placental concentrations of CD31, CD39, eNOS, VEGF, VEGFR1, and VEGFR2 between women with malignancies not receiving chemotherapy and the controls. In women receiving chemotherapy, IHC intensity and the number of positive cells were twice as high as in the control group. The activity of VEGFR1 and VEGFR2 was 11 times higher and 1.4 times higher, respectively, than in the control group. The mean number of cells expressing VEGFR1 and VEGFR2 per field of view increased by 1.5 times and 1.7 times, respectively. In addition, 1.6-fold reduction in CD31 level and 1.3-fold reduction in CD34 level as well as 1.4-fold increase in epithelial еNOS level and 1.3-fold increase in stromal eNOS level were revealed. Conclusions: our findings on IHC distribution of the expression of VEGF and its recep-tors in the placental tissue of pregnant women undergoing cytostatic chemotherapy in part illus-trate the processes of the compensation and impaired functioning of the mother-placentafetus system in pre-placental hypoxia. KEYWORDS: angiogenesis, vasculogenesis, vascular growth factor, chemotherapy, hypoxia, placental insufficiency. FOR CITATION: Yu.E. Dobrokhotova, Borovkova E.I., Arutyunyan A.M. et al. Placental vasculogenesis and angiogenesis in women undergoing chemotherapy. Russian Journal of Woman and Child Health. 2021;4(1):23–30. DOI: 10.32364/2618-8430-2021-4-1-23-30.

COMPARISON OF EFFICACY OF BEVACIZUMAB VS MITOMYCIN-C IN AUGMENTEDTRA BECULECTOMY

Background: Bevacizumab is inhibitor of vascular endothelial growth factor (VEGF), which plays a major role in physiological vasculogenesis and angiogenesis. Currently pegaptanib, ranibizumab and bevacizumab are the monoclonal antibodies used against VEGF. Aims: To compare the efficacy of subconjunctival bevacizumab to that of subtenonmitomycin-C (MMC) on the wound healing process in trabeculectomy. Materials and methods: Department of Ophthalmology, Command Hospital (Eastern Command), Kolkata. Patients of Primary Open Angle Glaucoma ( POAG). January 2016 –June 2017. Two groups: 30 in each group. (Calculated after assuming α error 0.05, power 80%). Randamization was done using website; www.graphpad.com/quickcalcs/index. patients were devided in two groups- Group A, who underwent trabeculectomy with mitomycin-C and group B, who underwent trabeculectomy with bevacizumab. Result & Analysis: In both groups intraocular pressure (IOP) was taken in preoperative, 01month, 06 month, 12 month and 18 month post operative period. Percentage decrease in IOP from pre-op is studied at 01, 06, 12 and 18 months. Conclusion: Glaucoma is a leading cause of irreversible blindness throughout the world. It has become the second most common cause of bilateral blindness. Lowering of the IOP is the first priority in POAG with anti glaucoma medications, however if patient’s IOP is uncontrolled with maximally tolerated antiglaucoma medications or there is noncompliance to anti glaucoma medications then patients can be planned for surgery to achieve target IOP. Trabeculectomy is the mainstay of surgical management of glaucoma.

A New Concept of the Pathogenesis of Retinopathy of Prematurity

The lecture provides a detailed description of the development of retinal vessels, vasculogenesis and angiogenesis. The cascade of protective mechanisms of the organism of the system of combating hyperoxia, the system of combating circulatory hypoxia and the key growth factors of the vascular endothelium during angiogenesis are shown. The pathogenesis of retinopathy of prematurity is described and the first phase of ROP development is analyzed in detail, the reasons for the delay in the maturation of vascular autoregulation are explained. The author proposed to distinguish the first preclinical phase in the ROP classification. In contrast to the modern concentration of attention of ophthalmologists on the active and cicatricial stages, the author proposes to pay special attention to the study of the preclinical stage of ROP, where its pathogenesis is formed.