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Iyoob, I.

Publications and source records attributed to Iyoob, I..

2 recordsLinked to original sources

Aging compromises Zebrafish caudal fin regeneration by disrupting Regenerative gene networks and Cellular metabolism

Zebrafish are widely recognized as a powerful vertebrate model for studying epimorphic regeneration due to their remarkable ability to restore complex tissues. However, regenerative efficiency declines with age, potentially due to alterations in gene regulatory networks and cellular metabolism. In the present study, we investigated the molecular and bioenergetic basis of age-associated regenerative decline by comparing young adult (<1 year) and old adult (>3 years) zebrafish during caudal fin regeneration. To further examine the contribution of mitochondrial function, mitochondrial dysfunction was experimentally induced using rotenone (20 nM), a mitochondrial Complex I inhibitor. Regenerative progression was assessed morphologically at 12hpa, 1dpa, 2dpa, 3dpa, and 7dpa, revealing a pronounced delay in fin regrowth in aged and rotenone-treated fish compared with young controls. Behavioral analysis indicated subtle but non-significant changes across experimental groups. Gene expression analysis using quantitative real-time PCR revealed age- and mitochondria-associated dysregulation of key regenerative gene families involved in developmental patterning, extracellular matrix organization, cellular signaling, and mitochondrial metabolism. Proteomic profiling further identified differential expression of proteins associated with mitochondrial bioenergetics, extracellular matrix remodeling, and signaling pathways required for blastema formation and tissue outgrowth. Ultrastructural examination by transmission electron microscopy revealed pronounced mitochondrial abnormalities, including enlarged mitochondria with fragmented or disrupted cristae, in aged and rotenone-treated regenerating tissues. Collectively, our integrative analysis establishes a mechanistic link between aging, mitochondrial dysfunction, and compromised regenerative capacity in zebrafish. The findings provide broader insights into metabolic constraints underlying age-related decline in regenerative potential in vertebrates.

developmental biology↗

Small molecule influence on Caudal fin regeneration in Zebrafish: A proteomic based study

Dietary and addictive small molecules play a significant role in altering in vivo conditions. Due to their minuscule size, these molecules can seamlessly traverse tissues and cellular membranes, influencing key biological processes such as cellular growth, differentiation, and intracellular communication, which are crucial for tissue regeneration. The zebrafish (Danio rerio) serves as an excellent model for studying regenerative growth due to its remarkable ability to regrow amputated appendages. In this study, we systematically evaluated the effect of small molecules, including ethanol (0.5%), glucose (1%), and NaCl (0.2%), on zebrafish caudal fin regeneration over a 7-day period. Regenerative growth analysis indicated delayed fin regrowth across all treated groups, with ethanol exposure showing the most significant impairment. Behavioural assessments revealed significant stress-induced locomotor alterations in treated groups, with the ethanol-exposed group exhibiting the most pronounced reduction in total distance moved and velocity. Proteomic profiling using label-free quantification (LFQ) identified 113, 257, and 178 differentially expressed proteins in ethanol, glucose, and NaCl-treated groups, respectively. Subsequent validation using the iTRAQ labeling approach confirmed 16 commonly dysregulated proteins across all conditions, highlighting a shared molecular response associated with stress and repair mechanisms. Pathway enrichment analysis mapped differentially expressed proteins to various canonical signaling pathways, including GP6 signaling, mitochondrial dysfunction, RHO GTPase cycling, antigen processing, and metabolic regulation. Ingenuity Pathway Analysis (IPA) further revealed associations with disease and function networks specific to each treatment condition. Our findings provide valuable insights into how metabolic and ionic perturbations influence zebrafish fin regeneration at the molecular level, offering a deeper understanding of tissue repair mechanisms under stressed conditions.

developmental biology↗