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Biology subjects

Chiou, Y.-T.

Publications and source records attributed to Chiou, Y.-T..

2 recordsLinked to original sources

De Novo Regeneration of Rete Ridges during Cetacean skin wound healing

Humans are tight-skinned mammals who typically fail to regenerate large full-thickness skin wounds, instead healing with substantial scarring and concomitant loss of function. Mechanical context is a major determinant of this outcome: elevated tissue tension or stiffness promotes fibrotic repair associated with hypertrophic or keloid scarring. Accordingly, regenerative medicine research has relied on diverse animal models to understand scar development and skin regeneration. Loose-skinned mammals exhibit greater regeneration ability. Furthermore, spiny mouse skin is significantly less stiff and associated with enhanced regenerative ability. Interestingly, this skin wound stiffness can be modulated to shift healing toward more regenerative or more fibrotic trajectories. Despite of this progress, the restoration of normal skin architecture after large-full thickness injury has not been elucidated in tight-skinned mammals. Can large full-thickness wounds regenerate with minimal scarring in tight-skinned mammals? Here we show the tight-skinned mammal Frasers Dolphin regenerates de novo a complex rete ridge architecture with associated vasculature and minimal scar following large full-thickness wound healing. Counterintuitively, this skin regeneration occurs in an aqueous, high-shear stress and high-tension environment. Complete rete ridge regeneration in tight-skinned mammals has not been documented and not observed in humans except in utero. This unique ability to rebuild elaborate rete ridges under tension is an opportunity to uncover molecular, cellular, and tissue-level mechanisms that enable regenerative wound healing in a mechanical regime typically associated with fibrosis.

pathology↗

Chemical-induced degradation of PreS2 mutant surface antigen reverses HBV- mediated hepatocarcinogenesis

Naturally evolved immune-escape PreS2 mutant is an oncogenic caveat of liver cirrhosis and hepatocellular carcinoma (HCC) during chronic hepatitis B virus (HBV) infection. Notably, PreS2 mutants is prevalent in above 50% of patients with HCC. Intrahepatic expression of PreS2 mutant large surface antigen (PreS2-LHBS) induces endoplasmic reticulum stress, mitochondria dysfunction, cytokinesis failure and subsequent chromosome hyperploidy. In this study, we ask if long-term inhibition of PreS2-LHBS may act to reverse HBV-mediated hepatocarcinogenesis. We set up a stability reporter platform and identified ABT199 as an inhibitor of PreS2-LHBS from a library of 1068 FDA-approved drugs. Treatment of ABT199 induced PreS2-LHBS degradation without affecting the general cell viability, as shown in hepatoma and immortalized hepatocyte cell lines. We found that ABT199 induced the recruitment of PreS2-LHBS to ring-shaped structures in close proximity to lysosomal marker Lamp1 and multivesicular body marker Rab7. Simultaneously, inhibitions of lysosomal degradation or microautophagy restored the expression of PreS2-LHBS. Specifically, a 24-hr treatment of ABT199 reduced DNA damages and cytokinesis failure induced by PreS2-LHBS. Persistent treatment of ABT199 for 3 weeks reversed chromosome hyperploidy in PreS2-LHBS cells and suppressed anchorage-independent growth of HBV-positive hepatoma cell line. Together, we showed that ABT199 provoked selective degradation of PreS2-LHBS through the induction of microautophagy, and a long-term treatment of ABT199 reversed oncogenic mechanisms induced by HBV. Our results indicate that long-term degradation of PreS2-LHBS may serve as a novel therapeutic strategy to constrain HBV-mediated hepatocarcinogenesis. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=66 SRC="FIGDIR/small/477454v1_ufig1.gif" ALT="Figure 1"> View larger version (16K): org.highwire.dtl.DTLVardef@1720c85org.highwire.dtl.DTLVardef@943121org.highwire.dtl.DTLVardef@1257a22org.highwire.dtl.DTLVardef@1756348_HPS_FORMAT_FIGEXP M_FIG C_FIG Author summaryHBV PreS2 mutant large surface antigen (PreS2-LHBS) is an oncoprotein that induces liver cirrhosis and liver cancer. This study identified ABT199 as a potential inhibitor of PreS2-LHBS. We found that ABT199 could trigger the degradation of PreS2-LHBS through the induction of microautophagy. Moreover, a long-term treatment of ABT199 significantly reversed LHBS-induced oncogenic events including DNA damage, mitotic failure, chromosome hyperploidy, and anchorage-independent growth. This study not only identifies a specific inhibitor of PreS2-LHBS but also highlights a plausible strategy to constrain HBV-mediated hepatocarcinogenesis through targeting the degradation of PreS2-LHBS.

microbiology↗