Publications by authors named "Kashmira Khaire"

The northern house gecko Hemidactylus flaviviridis exhibits appendage-specific responses to injuries. The autotomized tail regenerates, whereas the severed limb fails to regrow. Many site-specific cellular processes influence tail regeneration.

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Across the animal kingdom, lizards are the only amniotes capable of regenerating their lost tail through epimorphosis. Of the many reptiles, the northern house gecko, , is an excellent model system that is used for understanding the mechanism of epimorphic regeneration. A stage-specific transcriptome profile was generated in the current study following an autotomized tail with the HiSeq2500 platform.

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Article Synopsis
  • The study examines how COX-2 induced PGE impacts inflammation and wound healing in different body parts of a lizard, specifically the tail and limb.
  • During the early healing stage of the tail, increased levels of PGE and the EP4 receptor lead to a resolution of inflammation, reducing pro-inflammatory mediators and promoting IL-10, which aids healing.
  • In contrast, in the limb, COX-2 derived PGE maintains high levels of inflammation via EP2 receptor signaling, leading to prolonged elevation of pro-inflammatory mediators and reduced IL-10, which hampers wound healing and promotes scar formation.
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A recent study from our lab revealed that the inhibition of cyclooxygenase-2 (COX-2) exclusively reduces the level of PGE (Prostaglandin E) among prostanoids and hampers the normal development of several structures, strikingly the cranial vault, in chick embryos. In order to unearth the mechanism behind the deviant development of cranial features, the expression pattern of various factors that are known to influence cranial neural crest cell (CNCC) migration was checked in chick embryos after inhibiting COX-2 activity using etoricoxib. The compromised level of cell adhesion molecules and their upstream regulators, namely CDH1 (E-cadherin), CDH2 (N-cadherin), MSX1 (Msh homeobox 1), and TGF-β (Transforming growth factor beta), observed in the etoricoxib-treated embryos indicate that COX-2, through its downstream effector PGE, regulates the expression of these factors perhaps to aid the migration of CNCCs.

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Temporal expression patterns and activity of two cyclooxygenase (COX-1 and COX-2) isoforms were analysed during early chick embryogenesis to evaluate their roles in development. COX-2 inhibition with etoricoxib resulted in significant structural anomalies such as anophthalmia (born without one or both eyes), phocomelia (underdeveloped or truncated limbs), and gastroschisis (an opening in the abdominal wall), indicating its significance in embryogenesis. Furthermore, the levels of PGE, PGD, PGF, and TXB were assessed using quantitative LC-MS/MS to identify which effector prostanoid (s) had their synthesis initiated by COX-2.

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Exposure to chlorpyrifos-cypermethrin combination during early development resulted in defective looping and ventricular noncompaction of heart in domestic chicken. The study was extended to elucidate the molecular basis of this novel observation. The primary culture of chicken embryonic heart cells showed a concentration-dependent loss of viability when challenged with this combination of technical-grade insecticides.

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Article Synopsis
  • Chick embryonic cells are utilized to create a cost-effective in vitro model for studying muscle dystrophy (MD) by isolating and culturing limb myoblasts from 11-day-old chick embryos.
  • The addition of the anti-dystroglycan antibody (IIH6) disrupts the link between cytoskeletal proteins and the extracellular matrix, leading to observable changes in cell morphometry, contractibility, and signs of atrophy.
  • Gene expression analysis reveals increased TGF-β levels and decreased expression of muscle development genes, mirroring characteristics of MD, thus providing a platform for further research into the disease and potential treatments.
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