Publications by authors named "Antonion Korcari"
Tendon injuries are a major clinical problem, with poor patient outcomes caused by abundant scar tissue deposition during healing. Myofibroblasts play a critical role in the initial restoration of structural integrity after injury. However, persistent myofibroblast activity drives the transition to fibrotic scar tissue formation.
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- Tendon injuries often lead to complications due to excessive scar tissue and ineffective healing, primarily involving myofibroblasts, which are essential for initial recovery but can contribute to harmful fibrosis.
- Unlike previous strategies that focused on disrupting myofibroblast activity through targeting αSMA (a marker linked to various cell types), recent findings highlight that Periostin-lineage (Postn) cells play a vital role in creating a supportive environment for temporary myofibroblast activity necessary for proper tendon healing.
- Targeting the Periostin matrix could offer new therapeutic avenues to improve tendon healing by managing myofibroblast behavior and promoting regeneration instead of fibrosis.
Article Synopsis
- Tendons transmit force from muscles to bones, which is crucial for movement and their development relies on mechanical loading and calcium (Ca) signaling.
- The study focused on the Ca 1.2 voltage-gated Ca channel in tendon biology, revealing that it's highly expressed during tendon development but decreases in adults.
- Results showed that enhancing Ca 1.2 activity leads to larger tendons with increased collagen production and specific growth factors, suggesting that Ca signaling plays a critical role in tendon formation and remodeling.
Article Synopsis
- Tendons are key structures that connect muscles to bones, and their development and healing rely on mechanical loading and calcium (Ca) signaling, though specifics about Ca signaling in tendon cells remain unclear.
- In their study, researchers explored the role of the Ca 1.2 voltage-gated channel in tendon formation, finding it highly expressed during development but reduced in adults.
- Mice engineered to express a gain-of-function Ca 1.2 channel showed larger tendons with increased fibroblast numbers, enhanced collagen formation, and significant changes in extracellular matrix proteins and growth factors related to tendon development.
Article Synopsis
- Aged tendons experience disrupted balance, leading to higher injury risk and poor healing, highlighting the need to explore the underlying mechanisms for future treatments.
- Researchers created a new model using young mice (Scx-DTR) to mimic tendon aging, revealing similarities in cell loss and changes in the structure and composition of the tendon’s extracellular matrix (ECM).
- Findings show that while aged tenocytes become inflammatory and lose their ability to maintain protein balance, tenocytes from the Scx-DTR model can remodel effectively, suggesting potential targets for interventions to support tendon health throughout life.
Article Synopsis
- - ScxLin cells are the main cell type in tendons and are essential for tendon maintenance, but their role in tendon healing was unclear until this study examined their behavior during the healing process.
- - Researchers tracked ScxLin cells during healing and found that their population grows significantly until the early remodeling phase, but when these cells were depleted between days 14-18 post-surgery, tendon structure and function suffered at the 28-day mark.
- - RNA sequencing revealed that depleting ScxLin cells caused temporary stalling in the healing process, though by day 56, the tendon mechanics of the depleted group were similar to the normal healing group, highlighting the complex role of these cells in tendon repair.
Aging is a complex and progressive process where the tissues of the body demonstrate a decreased ability to maintain homeostasis. During aging, there are substantial cellular and molecular changes, with a subsequent increase in susceptibility to pathological degeneration of normal tissue function. In tendon, aging results in well characterized alterations in extracellular matrix (ECM) structure and composition.
View Article and Find Full Text PDFCharacterization of scar tissue biomechanics during adult murine flexor tendon healing.
J Mech Behav Biomed Mater
June 2022
Article Synopsis
- Tendon injuries are common and lead to mobility issues and lower quality of life due to scar tissue formation that is structurally weaker than healthy tendons.
- This study evaluates the mechanical properties of scar tissue in the flexor digitorum longus tendons during healing, revealing distinct differences compared to the surrounding composite healing tissue.
- The findings suggest that traditional methods of testing healing tendons may overestimate the properties of scar tissue, highlighting the need for targeted assessments to evaluate treatment effectiveness.
Article Synopsis
- Tendons play a role in various conditions, from birth defects to injuries, and understanding their development is crucial for advances in tissue engineering and regenerative medicine.
- The research focuses on the chick embryo as a model to study Achilles tendon development, overcoming challenges in accurately isolating and testing these small and delicate structures.
- A new "marking protocol" was created to enhance tendon isolation, revealing significant differences in mechanical properties compared to traditional methods, and aligning with previous findings on cell-level mechanics.
Despite the requirement for -lineage (Scx) cells during tendon development, the function of Scx cells during adult tendon repair, post-natal growth, and adult homeostasis have not been defined. Therefore, we inducibly depleted Scx cells (ScxLin) prior to tendon injury and repair surgery and hypothesized that ScxLin mice would exhibit functionally deficient healing compared to wild-type littermates. Surprisingly, depletion of Scx cells resulted in increased biomechanical properties without impairments in gliding function at 28 days post-repair, indicative of regeneration.
View Article and Find Full Text PDFThis erratum is to add the following paragraph in the Acknowledgement section.
View Article and Find Full Text PDFArticular cartilage is an avascular connective tissue responsible for bearing loads. Cell signaling plays a central role in cartilage homeostasis and tissue engineering by directing chondrocytes to synthesize/degrade the extracellular matrix or promote inflammatory responses. The aim of this paper was to investigate anabolic, catabolic and inflammatory pathways of well-known and underreported anabolic stimuli in 3D chondrocyte cultures and connect them to diverse cartilage responses including matrix regeneration and cell communication.
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