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Biology subjects

Tang, M.-J.

Publications and source records attributed to Tang, M.-J..

4 recordsLinked to original sources

Spatiotemporal secondary hair follicle development in the Lanyu pig (Sus scrofa taivanus): a novel pelage hair follicle model

Large full-thickness (LFT) skin wounds remain a major clinical challenge, and progress in regenerative medicine has been limited by poor translation from animal models to humans. A key limitation is that commonly used species such as mice, rats, and rabbits are loose-skinned, whereas humans are tight-skinned with distinct skin architecture. Although pigs more closely resemble human skin, widely used breeds have lost secondary (vellus-like) hair follicles through artificial selection, restricting their utility for studying ectodermal organ regeneration. Here, we characterize the development, patterning, and molecular features of secondary hair follicles in the Lanyu pig (Sus scrofa taivanus), an indigenous breed that retains these structures. Whole-mount and histological analyses revealed two distinct follicle populations: primary follicles arranged in stable triplet clusters and smaller secondary follicles distributed interstitially. A developmental time course using alkaline phosphatase (ALP) staining identified sequential stages of secondary follicle morphogenesis--placode, hair germ, hair peg, and mature follicle--occurring after primary follicle establishment. Immunohistochemical analysis demonstrated conserved epithelial- mesenchymal interactions, progressive epithelial stratification, and dynamic {beta}-catenin signaling during secondary follicle development. Keratin expression patterns and follicular architecture closely resembled those of human vellus hair follicles, supporting the translational relevance of this model. Notably, secondary follicles were retained into adulthood, and genetic analyses of outcrossed animals suggest that this trait follows an autosomal dominant inheritance pattern. Together, these findings establish the Lanyu pig as a tight-skinned mammalian model that preserves vellus-like hair follicles, providing a platform for investigating hair follicle-mediated skin regeneration and improving translational relevance for human wound healing.

developmental biology↗

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↗

Natural spider silk enhances mechanical performance of collagen scaffold under stretching conditions

Collagen is the most abundant protein in the extracellular matrix, crucial for wound healing and cell proliferation. While it holds promise as a scaffold for tendon, skin, and ligament reconstruction, collagens mechanical strength, particularly under stretch, is poor. Previous attempts to improve collagen strength involved blending it with silkworm or recombinant spider silk. In this study, for the first time, we evaluated whether collagen gel from fish skin could be strengthened by infusing it with native spider silk, specifically the major ampullate (MA) silk of Nephila pilipes, known for superior mechanical properties. MA silk was woven onto a frame, pressed into a PDMS platform, and then used to create a collagen scaffold. Youngs modulus of the infused collagen scaffold, subjected to either stretching or non-stretching treatments, was measured using AFM. After 24 hours of cyclic stretching, collagen infused with silk showed less fragility, higher Youngs modulus, and no bacterial growth. Immunohistochemical staining showed that after stretching, the thickness and architecture of the collagen gel infused with silk were maintained, and the fibers were reorganized in a more compact, aligned, and denser manner. Overall, collagen infused with native spider silk exhibited improved mechanical stability and stiffness under cyclic stretching, suggesting that this combination could serve as a robust matrix for bioengineering applications while preventing bacterial infiltration.

zoology↗

Depletion of tropomyosin 1.6 promotes matrix-degrading phenotype in TGF-β1-induced myofibroblast

Fibroblasts can be transformed into myofibroblasts under pro-fibrotic conditions, which is characterized by increased contractility and reduced matrix degradation. The relationship between contractile activity and matrix degradation is not fully understood. We found that TGF-{beta}1-induced myofibroblast activation occurs on a culture dish, favoring stress fiber formation and inhibiting podosome structures due to high matrix stiffness. To mimic physiological conditions, we cultured fibroblasts on collagen gel. Blocking actomyosin signaling significantly reduced TGF-{beta}1-induced myofibroblast activation. Tpm1.6, an actomyosin-associated contractile unit, was specifically upregulated by TGF-{beta}1 on soft collagen substrates. Depletion of Tpm1.6 attenuated TGF-{beta}1-induced increase of -SMA, N-cadherin, and {beta}1-integrin, indicating its crucial role in early myofibroblast activation during fibrosis progression. Tpm1.6 depletion reduced TGF-{beta}1-induced cell contractility and enhanced collagen degradation. Notably, in Tpm1.6-depleted fibroblasts, TGF-{beta}1 triggered formation of distinct -SMA dot structures enriched with MMP9, promoting collagen degradation. Our study highlights the pivotal role of Tpm1.6 in TGF-{beta}1-induced myofibroblast activation and collagen degradation. Depletion of Tpm1.6 triggers robust collagen degradation through distinct -SMA dots, presenting a potential therapeutic approach for chronic kidney disease.

cell biology↗