Publications by authors named "Neha Deshpande"

Fuchs Endothelial Corneal Dystrophy (FECD) is an aging disorder characterized by expedited loss of corneal endothelial cells (CEnCs) and heightened DNA damage compared to normal CEnCs. We previously established that ultraviolet-A (UVA) light causes DNA damage and leads to FECD phenotype in a non-genetic mouse model. Here, we demonstrate that acute treatment with chemical stressor, menadione, or physiological stressors, UVA, and catechol estrogen (4-OHE), results in an early and increased activation of ATM-mediated DNA damage response in FECD compared to normal CEnCs.

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  • Epidemiological studies indicate that cigarette smoking worsens corneal endothelial dysfunction, but the exact reasons are not well understood.
  • The research found that prolonged exposure to smoke activates the aryl hydrocarbon receptor (AhR), which increases the expression of CYP1B1 and leads to aging and scarring in corneal cells, possibly as a way to adapt to damage.
  • While these changes suggest early signs of dysfunction, no severe damage was detected, implying that developing a serious condition like Fuchs endothelial corneal dystrophy requires other environmental or genetic influences beyond just smoking.
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Fuchs endothelial corneal dystrophy is a heterogenous disease with multifactorial etiology, and genetic, epigenetic, and exogenous factors contributing to its pathogenesis. DNA damage plays a significant role, with ultraviolet-A (UV-A) emerging as a key contributing factor. We investigate the potential application of neuropeptide α-melanocyte stimulating hormone (α-MSH) in mitigating oxidative stress induced endothelial damage.

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  • Descemet's Stripping Only (DSO) is a surgical technique that relies on the migration of corneal endothelial cells (CEnCs) to close wounds, and ripasudil, a ROCK inhibitor, may enhance this process.
  • Research found that ripasudil significantly improves the migration and wound healing of both normal and Fuchs endothelial corneal dystrophy (FECD) cells, specifically boosting the activity of certain proteins associated with cell mobility.
  • Ex vivo experiments showed that ripasudil treatment led to better migration and proliferation of CEnCs, suggesting it could be a valuable addition to DSO procedures by improving healing outcomes in the corneal environment.
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Fuchs endothelial corneal dystrophy (FECD) is a genetically complex, age-related, female-predominant disorder characterized by loss of post-mitotic corneal endothelial cells (CEnCs). Ultraviolet-A (UVA) light has been shown to recapitulate the morphological and molecular changes seen in FECD to a greater extent in females than males, by triggering CYP1B1 upregulation in females. Herein, we investigated the mechanism of greater CEnC susceptibility to UVA in females by studying estrogen metabolism in response to UVA in the cornea.

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Corneal endothelial cells (CEnCs) regulate corneal hydration and maintain tissue transparency through their barrier and pump function. However, these cells exhibit limited regenerative capacity following injury. Currently, corneal transplantation is the only established therapy for restoring endothelial function, and there are no pharmacologic interventions available for restoring endothelial function.

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Background: To evaluate and compare efficacy of pinhole surgical technique (PST) alone and with advanced platelet rich fibrin (A-PRF) in the management of bilateral multiple adjacent gingival recession defects (MAGRD).

Methods: One hundred and sixty five MAGRD were randomly assigned to control group (treated with PST) and test group (PST with A-PRF). Clinical parameters of gingival recession depth (GRD), gingival recession width (GRW), width of keratinised gingiva (WKG), complete root coverage (CRC) and gingival thickness (GT) on ST-CBCT was measured at 2, 4 and 6 mm apically from the gingival margin.

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Fuchs Endothelial Corneal Dystrophy (FECD), a late-onset oxidative stress disorder, is the most common cause of corneal endothelial degeneration and is genetically associated with CTG repeat expansion in Transcription Factor 4 (TCF4). We previously reported accumulation of nuclear (nDNA) and mitochondrial (mtDNA) damage in FECD. Specifically, mtDNA damage was a prominent finding in development of disease in the ultraviolet-A (UVA) induced FECD mouse model.

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Gene transcription is an essential and highly regulated process. In eukaryotic cells, the structural organization of nucleosomes with DNA wrapped around histone proteins impedes transcription. Chromatin remodelers, transcription factors, co-activators, and histone-modifying enzymes work together to make DNA accessible to RNA polymerase.

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Over the past decades, reactions involving C-H functionalization have become a hot theme in organic transformations because they have a lot of potential for the streamlined synthesis of complex molecules. C(sp)-H bonds are present in most organic species. Since organic molecules have massive significance in various aspects of life, the exploitation and functionalization of C(sp)-H bonds hold enormous importance.

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  • - The study investigated how gender affects the relationship between gingival display and lip dimensions, intercommissural width (ICW), interdental smile line (ISL), and gingival smile line (GSL) in healthy individuals.
  • - Researchers measured lip length, ICW, and gingival characteristics in 120 participants aged 20-40, finding significant differences in lip positions and gingival displays between males and females.
  • - The findings suggest that understanding these gender-related differences could enhance aesthetic procedures in dentistry by tailoring them to individual characteristics.
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Mono-methylation of the fourth lysine on the N-terminal tail of histone H3 was found to support the induction of RNA polymerase II transcription in S. cerevisiae during nutrient stress. In S.

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Attachment to the matrix is critical for the survival of adherent cells, whereas detachment triggers death by apoptosis. Therefore, solid tumors must acquire the ability to survive the stress of matrix-detachment to transit through circulation and seed metastases. Although a central role for energy metabolism in cancer progression is well established, what distinguishes its role in the cellular state of the matrix-deprived form compared to the matrix-attached form is not fully understood yet.

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  • The study investigates the migration speeds of corneal endothelial cells (CECs) in patients with Fuchs endothelial corneal dystrophy (FECD) compared to normal controls.
  • It utilizes live cell imaging and scratch assays to measure cellular migration under different conditions, analyzing specimens from FECD patients and normal cadaveric donors.
  • Results show that FECD CECs have significantly higher migration speeds in both low and high cell density conditions compared to normal CECs, indicating altered cellular behavior in FECD.
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Fuchs endothelial corneal dystrophy (FECD) is an age-related disease whereby progressive loss of corneal endothelial cells (CEnCs) leads to loss of vision. There is currently a lack of therapeutic interventions as the etiology of the disease is complex, with both genetic and environmental factors. In this study, we have provided further insights into the pathogenesis of the disease, showing a causal relationship between senescence and endothelial-mesenchymal transition (EMT) using in vitro and in vivo models.

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T cells express clonotypic T cell receptors (TCRs) that recognize peptide antigens in the context of class I or II MHC molecules (pMHCI/II). These receptor modules associate with three signaling modules (CD3γε, δε, and ζζ) and work in concert with a coreceptor module (either CD8 or CD4) to drive T cell activation in response to pMHCI/II. Here, we describe a first-generation biomimetic five-module chimeric antigen receptor (CAR).

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A key difference that distinguishes viral infections from protein immunizations is the recognition of viral nucleic acids by cytosolic pattern recognition receptors (PRRs). Insights into the functions of cytosolic PRRs such as the RNA-sensing Rig-I-like receptors (RLRs) in the instruction of adaptive immunity are therefore critical to understand protective immunity to infections. West Nile virus (WNV) infection of mice deficent of RLR-signaling adaptor MAVS results in a defective adaptive immune response.

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Fuchs Endothelial Corneal Dystrophy (FECD) is an age-related genetically complex disease characterized by increased oxidative DNA damage and progressive degeneration of corneal endothelial cells (HCEnCs). FECD has a greater incidence and advanced phenotype in women, suggesting a possible role of hormones in the sex-driven differences seen in the disease pathogenesis. In this study, catechol estrogen (4-OHE), the byproduct of estrogen metabolism, induced genotoxic estrogen-DNA adducts formation, macromolecular DNA damage, and apoptotic cell death in HCEnCs; these findings were potentiated by menadione (MN)-mediated reactive oxygen species (ROS).

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Fuchs endothelial corneal dystrophy (FECD) is a leading cause of corneal endothelial (CE) degeneration resulting in impaired visual acuity. It is a genetically complex and age-related disorder, with higher incidence in females. In this study, we established a nongenetic FECD animal model based on the physiologic outcome of CE susceptibility to oxidative stress by demonstrating that corneal exposure to ultraviolet A (UVA) recapitulates the morphological and molecular changes of FECD.

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Corneal endothelium (CE) is a monolayer of mitochondria-rich cells, critical for maintaining corneal transparency compatible with clear vision. Fuchs endothelial corneal dystrophy (FECD) is a heterogeneous, genetically complex disorder, where oxidative stress plays a key role in the rosette formation during the degenerative loss of CE. Increased mitochondrial fragmentation along with excessive mitophagy activation has been detected in FECD; however, the mechanism of aberrant mitochondrial dynamics in CE cell loss is poorly understood.

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Intentional replantation has been used as an alternative treatment modality to tooth extraction and prosthetic replacement when conventional endodontic treatment modalities are unfeasible or contraindicated. This case report presents a successful case of intentional replantation for the mandibular first molar with an endodontic mishap. An endodontic instrument was separated in the apical third of the root canal and extended beyond its mesiobuccal root apex.

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