Biology subjects

Peng, C.-C.

Publications and source records attributed to Peng, C.-C..

3 recordsLinked to original sources

bioRxiv2026

Extracellular Vesicle Biomarkers in the Aqueous Humor Correlate with Retinoblastoma Seeding

PurposeTo investigate the correlation of retinoblastoma (RB) aqueous humor (AH)-derived extracellular vesicle (EV) surface markers, particularly CD133, with clinical features of RB. MethodsAH samples (n=22) collected at diagnosis (n=17) or primary enucleation (n=5) from RB eyes were profiled using magnetic bead-based flow cytometry. Median fluorescence intensities (MFI) of tetraspanins (CD9, CD63, CD81) and CD133 were quantified and correlated with International Intraocular RB Classification (IIRC) stage, seeding location, seeding morphology, and enucleation. ResultsCD133+ EVs were detected in 16 of 22 (73%) samples. While CD133 levels showed a non-significant increasing trend with advanced IIRC stages, CD133 expression was significantly elevated in eyes with vitreous seeding vs. subretinal only (P = 0.010). Cuzicks trend analysis revealed a significant association between rising CD133 % MFI and complex seeding (P < 0.001). Conversely, CD63 displayed a significant inverse trend, with decreasing % MFI associated with complex seeding (P < 0.001). CD133high eyes (MFI>10,000, n=9) exhibited increased enucleation (P = 0.007) and predominantly sphere/cloud seeding patterns (P = 0.001). CD133high eyes demonstrated a coordinated CD63/CD81 co-expression pattern (r = 0.80), absent in the CD133low group. ConclusionsElevated CD133 level and percentage were associated with vitreous involvement and complex seeding morphology, suggesting potential as a minimally invasive indicator of disease burden. The inverse relationship between CD63 and seeding severity, combined with CD63/CD81 remodeling in CD133high eyes, suggests an EV profile indicative of aggressive disease. These findings support the association of CD133+ EVs with advanced RB seeding and warrant further prospective validation.

cancer biology↗

bioRxiv2025

Small shifts, big ripples: multi-omics studies reveal how ambient temperatures govern Chlamydomonas cellular responses

Photosynthetic protists, known as microalgae, face increasing temperatures due to climate change. The green biflagellate alga Chlamydomonas reinhardtii serves as a model for thermoregulation. While responses to thermal stress are well characterized, much less is known about the impact of ambient temperature shifts. Understanding microalgal responses to environmental temperature changes is critical, as these primary producers drive ecosystem productivity and food web dynamics. Here, C. reinhardtii grew mixotrophically at ambient temperatures from 18 {degrees}C to 33 {degrees}C. Transcriptomic profiling revealed extensive reorganization, with over 5,000 transcripts significantly affected, including those involved in algal-bacterial interactions, photoreception, lipid metabolism, photosynthesis, cilia formation, and the secretome. CO2 transfer rates and acetate levels measured at 18 {degrees}C and 28 {degrees}C suggest decreased photoautotrophic algal growth at 28 {degrees}C at first. Antagonistic bacterial activity was sustained longer at lower temperatures. Proteomic analyses of isolated cilia and secreted proteins corroborate major abundance changes within these sub-proteomes, particularly in ciliary intraflagellar transport complexes and mating-related proteins in the secretome. Together, these molecular alterations resulted in pronounced changes in growth, the lengths of cells and cilia swimming behavior, mating ability and bacterial antagonism. These data reveal major cellular responses caused by ambient, even short-term temperature shifts.

cell biology↗

bioRxiv2018

Nifedipine Modulated Renal Lipogenesis via AMPK-SREBP Transcriptional Pathways

Lipid accumulation in renal cells has been implicated in the pathogenesis of obesity-related kidney disease, and lipotoxicity occurring in the kidney can be a surrogate marker for renal failure or renal fibrosis. Nifedipine-induced renal lipotoxicity has never been cited, although a few studies have shown that nifedipine inhibits lipogenesis via activation of the LKB1-AMPK pathway. Therefore, we utilized NRK52E cell models to examine this further. We pre-treated cells with varying concentrations of nifedipine (7.5, 15, or 30 M) for 24 or 48 h prior to examining the activity of lipogenesis enzymes and lipotoxicity.\n\nNifedipine was found to activate acetyl CoA synthetase, acetyl CoA carboxylase, long chain fatty acyl CoA elongase, ATP-citrate lyase, and HMG CoA reductase, suggesting elevated production of cholesterol, triacylglycerides, and phospholipids. Nifedipine exposure induced a vast accumulation of cytosolic free fatty acids (FFA) and stimulated the production of reactive oxygen species, upregulated CD36 and KIM-1 (kidney injury molecule-1) expression, inhibited p-AMPK activity, and triggered the transcription of SREBP-1/2 and lipin-1, underscoring the potential of nifedipine to induce lipotoxicity with renal damage.\n\nIn the present study, we elucidated the mechanism of action of nifedipine that leads to renal lipotoxicity via the AMPK-SREBP-1/2 pathway. To our knowledge, this is the first report demonstrating nifedipine-induced lipid accumulation in the kidney.

biochemistry↗