Retinal pericytes (PCs) are contractile microvascular smooth muscle cells that wrap around the endothelial cells (ECs) maintaining intact retinal vasculature (RV) with a 1:1 ratio. Microvascular complications like diabetic retinopathy (DR) due to chronic diabetes causes apoptotic loss of PCs followed by diminished vessel stability, EC apoptosis, and ischemia, leading to retinal angiogenesis, and eventually severe vision loss. This study aimed to analyze the proteins in PCs isolated from the RV of diabetic human donor eyes and compare them with remaining mixed population (MP) of retinal vascular cells.
View Article and Find Full Text PDFDiabetic Retinopathy is prevalent among patients with uncontrolled hyperglycemia resulting in vision loss. Despite numerous challenges to create a link among these conditions, the characterization of pathological neovascularization causing retinal damage due to the prognosis of early non-proliferative diabetic retinopathy to late proliferative diabetic retinopathy needs deep understanding. In this study, meta-analysis-based integration of gene expression datasets for the fibrovascular membrane of PDR and neural retina of NPDR were compared, to investigate the differentially expressed genes involved in retinal angiogenesis.
View Article and Find Full Text PDFPurpose: To evaluate and correlate retinal microvascular changes in prediabetic and diabetic patients with functional and systemic parameters.
Methods: Optical coherence tomography angiography (OCTA) was performed on all subjects after medical evaluation and laboratory investigations for blood sugar, glycosylated hemoglobin, and others. Automated quantification of vascular indices of the superficial plexus were analyzed.
Pericytes (PC) are microvascular mural cells that make specific cell-to-cell contacts with the endothelial cells (EC). These cells are obligatory constituents of the microvessels including the retinal vasculature and they serve as regulators of vascular development, stabilization, maturation and remodeling. During early stages of diabetic retinopathy (DR), apoptotic loss of PC surrounding the retinal vasculature occurs.
View Article and Find Full Text PDFPurpose: This study was undertaken to investigate the neurovascular changes in the retina of prediabetic subjects.
Methods: Subjects enroled in a prospective study were separated into prediabetic and normal control groups based on their glycosylated haemoglobin (HbA1C) levels, fasting and postprandial blood sugar levels and glucose tolerance test. All the subjects underwent detailed ophthalmic evaluation, which included fundus examination, fundus photography, optical coherence tomography angiography (OCTA), and multifocal electroretinogram (mfERG).
Purpose: To evaluate the differences in vascular indices in different scan sizes of optical coherence tomography angiography (OCTA) images in normal persons versus persons with diabetic retinopathy.
Methods: OCTA scans of diabetic patients and age-matched controls were performed by a single operator. Automated quantification of vascular indices of the superficial plexus was analyzed in two angiocubes of 3 × 3 mm and 6 × 6 mm, respectively.
Hyperlipidemia is associated with the progression of diabetic retinopathy (DR). Paraoxonase 1 (PON1), an esterase is known to prevent systemic LDL oxidation. This study assessed if serum oxLDL is associated with the progression of Type 2 DM to DR.
View Article and Find Full Text PDFObjective: The study was conducted to observe the serum and vitreous levels of LXA4, BDNF and Th1/Th2 cytokines in type 2 diabetes mellitus (DM) and changes associated with diabetic retinopathy (DR). Further, the in vitro study was performed to analyze the exposure of BDNF and LXA4 on LPS-induced pro-inflammatory state in ARPE 19 cells.
Materials And Methods: Totally 114 individuals were recruited in a prospective case control study.
Background: Brain-derived neurotrophic factor (BDNF) is a potent neurotrophic factor that is implicated in the regulation of food intake and body weight. Polyunsaturated fatty acids (PUFAs) localised in cell membranes have been shown to alter the levels of BDNF in the brain, suggesting that PUFAs and BDNF could have physical interaction with each other. To decipher the molecular mechanism through which PUFAs modulates BDNF's activity, molecular docking was performed for BDNF with PUFAs and its metabolites, with 4-Methyl Catechol as a control.
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