为深化中韩两国在哺乳动物组织修复与器官再生领域的学术交流，借鉴前沿基础研究成果，助力鹿茸再生机制解析，长春科技学院鹿茸科学与产品技术研究所、吉林大学第二附属医院、吉林省中韩动物科学研究院联合举办2026中韩哺乳动物器官再生研讨会。现将有关事宜通知如下：
01组织单位
主办单位：
长春科技学院鹿茸科学与产品技术研究所、吉林大学第二附属医院、吉林省中韩动物科学研究院
02会议时间
2026年7月10日 9：00-15：00
03会议地点
长春科技学院鹿茸科学与产品技术研究所学术报告厅
特邀主旨报告专家
Hanseul Yang
Organization: Department of Biological Science, KAIST, Republic of Korea
Title: Made to be Broken: The Architecture and Functions of Skin Fracture Lattice in Spiny Mice
Abstract: Autotomy is a unique phenotype whereby an animal sheds a body part to escape predation. The timing and location of autotomy are tightly regulated by preformed planes of weakness (aka fracture planes), which facilitate tissue loss. While autotomy is often followed by regeneration, these phenotypes are rarely reported in mammals. A notable exception is spiny mice (Acomys), which exhibit skin autotomy and, more remarkably, complete tissue regeneration. Presently, the mechanisms underlying autotomy and complete regeneration in Acomys skin remain elusive. Here, we report the discovery of a honeycomb-like fracture lattice in Acomys skin whose design directs tissue destruction but also facilitates regenerative healing. Unlike the single continuous surface of a fracture plane, this fracture lattice consists of a three-dimensional array of hexagonal units whose boundaries guide tissue breakage. Moreover, we identify collagen VI as the main constituent of the fracture lattice and find that it is distinctly arranged to initiate fracturing and propagation of skin tearing. By preconditioning the tissue for autotomy, the fracture lattice dampens the damage-induced inflammatory response but also upregulates a pro-regenerative gene signature, accelerating skin appendage regeneration. Lastly, we discovered the key role of spiny hairs in fracture lattice formation, as inhibiting their development leads to abnormal pattern formation and changes in skin fracture mechanics. Our results present a novel example of a uniquely evolved structural adaptation in mammalian skin that links tissue patterning, autotomy, and regeneration. We expect that the application of a modular compartment structure to artificial skin and other organ engineering may enhance resilience to injury and facilitate efficient regeneration.
张国坤
长科鹿茸研究所
题目：CCL3调控哺乳动物断肢再生
摘要：哺乳动物断肢再生能力极为有限，小鼠P3趾尖与鹿茸作为特例，深入解析其关键调控机制对诱导人类断肢再生具有重要意义。本研究通过小鼠P3趾尖再生的单细胞测序数据发现，CCL3是再生芽基形成的关键调控因子；同时，鹿茸再生芽基祖细胞检测结果也显示出相似的表达模式，提示CCL3在哺乳动物断肢再生中可能具有进化保守的共性作用。为验证这一发现，我们构建了CCL3基因敲除（CCL3-KO）小鼠模型，结果显示敲除CCL3后小鼠P3趾尖再生失败。机制研究表明，CCL3缺失显著影响了巨噬细胞对芽基细胞的招募，并抑制了芽基细胞再生表型的获得，表现为芽基标志基因表达减弱及细胞可塑性降低。进一步实验证实，外源性CCL3重组蛋白的补充能够有效恢复CCL3-KO小鼠P3趾尖的再生能力。本研究揭示了CCL3通过调控巨噬细胞介导的芽基细胞招募及芽基细胞再生表型建立，在哺乳动物断肢再生过程中发挥不可或缺的关键作用，为临床促进断肢再生提供了潜在的干预靶点。
Title: CCL3 Regulates Mammalian Limb Regeneration
Abstract: Mammalian limb regeneration is extremely limited, with mouse P3 digit tips and antlers representing notable exceptions. Elucidating the key regulatory mechanisms underlying these exceptional regenerative capacities holds significant implications for inducing human limb regeneration. In this study, single-cell sequencing data from mouse P3 digit tip regeneration revealed that CCL3 is a critical regulator of blastema formation. Concurrently, analysis of antler regeneration blastema progenitor cells revealed a similar expression pattern, suggesting that CCL3 may play an evolutionarily conserved role in mammalian limb regeneration. To validate this finding, we generated CCL3 knockout (CCL3-KO) mice and demonstrated that CCL3 deficiency resulted in failed P3 digit tip regeneration. Mechanistic studies indicated that CCL3 loss significantly impaired macrophage-mediated recruitment of blastema cells and suppressed the acquisition of regenerative phenotypes, as evidenced by downregulated blastema marker gene expression and diminished cellular plasticity. Furthermore, exogenous supplementation with recombinant CCL3 protein effectively restored the regenerative capacity of P3 digit tips in CCL3-KO mice. Overall, this study reveals that CCL3 plays an indispensable role in mammalian limb regeneration by regulating macrophage-mediated blastema cell recruitment and the establishment of blastema cell regenerative phenotypes, providing a potential therapeutic target for clinical promotion of limb regeneration.
刘贺
吉大二院
题目：受鹿茸逆向成骨启发——TNC富集的基质囊泡促进骨质疏松骨再生
摘要：鹿生茸期全身呈骨吸收优势，而鹿茸局部却大量新骨形成，提示其中存在独特的成骨调控机制。受鹿茸周期性再生及“逆向成骨”现象启发，本研究旨在探索骨质疏松背景下实现局部快速成骨的新策略，聚焦于矿化启动关键结构——基质囊泡，系统筛选鹿茸不同区域及粘附特性的囊泡亚群，发现成骨区粘附型基质囊泡促成骨活性最强。体外实验显示，该囊泡可显著加速大鼠骨髓间充质干细胞成骨分化，3天内即出现Runx2、OCN高表达及矿化结节形成；转录组学证实其早期激活Wnt、MAPK等成骨通路。体内实验中，静脉注射或水凝胶负载该囊泡均能有效修复去卵巢骨质疏松小鼠的骨缺损，恢复骨量。蛋白质组学筛选出关键效应分子肌腱蛋白C（TNC），基因敲除实验表明TNC缺失显著抑制成骨分化及细胞外基质相关基因表达，提示TNC可能通过调控靶细胞周围微环境参与成骨调控。本研究为骨质疏松骨再生提供了新思路和潜在治疗工具。
Title: Inspired by the Reverse Osteogenesis of Deer Antlers—TNC-Enriched Matrix Vesicles Promote Bone Regeneration in Osteoporosis.
Abstract: During antler growth, deer exhibit systemic bone resorption dominance, while substantial new bone formation occurs locally in the antlers, implying the existence of a unique osteogenic regulatory mechanism. Inspired by the periodic regeneration of deer antlers and the "reverse osteogenesis" phenomenon, this study aimed to explore novel strategies for achieving rapid localized bone formation under osteoporotic conditions. Focusing on matrix vesicles—the key structures that initiate mineralization—we systematically screened vesicle subpopulations from different antler regions and categorized them based on their attachment properties. We identified that attached matrix vesicles derived from the osteogenic zone exhibited the strongest osteogenic-inducing activity. In vitro experiments demonstrated that these vesicles significantly accelerated the osteogenic differentiation of rat bone marrow mesenchymal stem cells, as evidenced by high Runx2 and OCN expression and mineralized nodule formation within 3 days. Transcriptomic analysis confirmed the early activation of osteogenic pathways, including the Wnt and MAPK signaling cascades. In vivo results showed that intravenous injection or hydrogel-loaded delivery of the vesicles effectively restored bone mass in osteoporotic mice and repaired bone defects in osteoporotic rats. Proteomic screening identified tenascin-C (TNC) as a key effector molecule; gene knockout experiments revealed that TNC deficiency significantly inhibited osteogenic differentiation and the expression of extracellular matrix-related genes, suggesting that TNC may regulate osteogenesis by modulating the extracellular matrix microenvironment surrounding target cells. Collectively, this study provides new theoretical insights and potential therapeutic strategies for bone regeneration in osteoporosis.
张家鑫
吉大二院
题目：离子交换调控的Ca⟡⁺/ZA协同释放重建成骨-破骨耦联并促进骨质疏松骨整合
摘要：骨质疏松状态下假体与宿主骨整合受限，导致术后假体松动等并发症高发。课题组前期通过局部负载唑来膦酸（ZA）显著改善了骨质疏松植入物骨整合，但仍存在骨整合失效现象。究其原因，ZA虽可有效抑制破骨细胞活性，但持续抗破骨作用会影响成骨-破骨耦联，削弱界面骨基质沉积和矿化成熟，从而限制骨质疏松植入物骨整合。本研究构建了一种Ca⟡⁺功能化多级孔分子筛-ZA涂层（Ti-HZ-Ca/ZA）能够实现植入物界面发挥抗破骨与促成骨的协同作用。该涂层通过介孔结构负载弱吸附ZA以提供早期抗骨吸收作用，同时利用分子筛骨架中可交换的Ca⟡⁺与ZA膦酸基团形成Ca-ZA配位结合；在含Na⁺微环境中，Na⁺/Ca⟡⁺交换机制驱动Ca结合态ZA和生物活性Ca⟡⁺协同释放。Ti-HZ-Ca/ZA涂层显著抑制破骨细胞分化、封闭区形成和骨吸收，同时维持骨髓间充质干细胞活性并促进成骨分化和基质矿化。在成骨-破骨共培养体系中，该涂层降低RANKL/OPG比值，并激活以细胞外基质为核心的基质黏附与矿化成熟，实现了平衡成骨-破骨耦联的生物学功能。进一步骨质疏松动物模型中，Ti-HZ-Ca/ZA显著改善假体周围成熟矿化骨形成、骨-植入物界面整合和力学性能，且未见明显系统毒性。该研究提出了一种通过动态Ca⟡⁺/ZA协同释放缓解ZA相关成骨-破骨失衡的局部界面调控策略，为改善骨质疏松植入物长期稳定性提供了新的临床转化思路。
Title:Ion-exchange-regulated Ca⟡⁺/zoledronic acid co-release restores osteoblast–osteoclast coupling for osteoporotic osseointegration
Abstract: Osteoporosis compromises implant–host bone integration and increases the incidence of postoperative complications such as implant loosening. In our previous work, local delivery of zoledronic acid (ZA) markedly improved osteoporotic implant osseointegration; however, a subset of implants still exhibited insufficient bone integration. Mechanistically, although ZA effectively suppresses osteoclast activity, sustained antiresorptive exposure may disrupt osteoblast–osteoclast coupling, impair interfacial bone matrix deposition and mineral maturation, and thereby limit osseointegration under osteoporotic conditions. Here, we developed a Ca⟡⁺-functionalized hierarchical zeolite-ZA coating on porous titanium implants, termed Ti-HZ-Ca/ZA, to coordinate antiresorptive activity with osteogenic repair at the implant interface. The mesoporous structure of the coating enabled the loading of weakly adsorbed ZA for early antiresorptive release, whereas exchangeable Ca⟡⁺ within the zeolite framework coordinated with the phosphonate groups of ZA to form Ca-ZA complexes. In a Na⁺-containing microenvironment, Na⁺/Ca⟡⁺ exchange drove the coordinated release of Ca-bound ZA and bioactive Ca⟡⁺. Ti-HZ-Ca/ZA significantly inhibited osteoclast differentiation, sealing-zone formation and bone resorption, while preserving the viability of BMSCs, promoting osteogenic differentiation and matrix mineralization. In an osteoblast–osteoclast co-culture system, the coating reduced the RANKL/OPG ratio and activated an extracellular matrix-centered program associated with matrix adhesion and mineral maturation, indicating restoration of osteoblast-osteoclast coupling. Furthermore, in an osteoporotic animal, Ti-HZ-Ca/ZA markedly enhanced mature mineralized bone formation, bone-implant interfacial integration and biomechanical performance without detectable systemic toxicity. Collectively, this study proposes a local interface-regulation strategy in which dynamic Ca⟡⁺/ZA co-release alleviates ZA-associated osteoblast-osteoclast uncoupling, providing a translational approach for improving the long-term stability of osteoporotic implants.
初审：李春义
复审：陈浩
终审：孟祥杰
