Synapses are inter-neuronal connections that are fundamental working units in neural networks. How synapses are molecularly constructed is a fascinating question, which attracted scientists' attention for many decades. Neuromuscular junction, a field pioneered by Te-Pei FENG and many others, has been an excellent model for studying synaptogenesis and paved the way for our understanding of the synapse formation in the central nervous system. Recent studies shed new light on the molecular mechanisms of central synapse formation by discovering a group of cell adhesion molecules exerting potent synaptogenic effects. This review will focus on those cell adhesion molecules which can induce central synapse formation when expressed in non-neuronal cells.
Cell Adhesion ; Cell Adhesion Molecules ; physiology ; Humans ; Neuromuscular Junction ; physiology ; Synapses ; physiology

Synaptic cell adhesion molecules (CAMs) are a type of membrane surface glycoproteins that mediate the structural and functional interactions between pre- and post-synaptic sites. Synaptic CAMs dynamically regulate synaptic activity and plasticity, and their expression and function are modulated by environmental factors. Synaptic CAMs are also important effector molecules of stress response, and mediate the adverse impact of stress on cognition and emotion. In this review, we will summarize the recent progress on the role of synaptic CAMs in stress, and aim to provide insight into the molecular mechanisms and drug development of stress-related disorders.
Cell Adhesion ; Cell Adhesion Molecules ; physiology ; Humans ; Neuronal Plasticity ; Stress, Physiological ; Stress, Psychological ; Synapses

Fetal wound healing has drawn the attention of many researchers from diverse background and specialties. Fetal wound healing is unique and differs from postnatal healing in that fetal skin wounds heal rapidly without scar formation. If the mechanism underlying such phenomenon can be elucidated, it will be serve as a significant milestone in the study of wound healing. Furthermore, the implications for therapeutic applications in wound management and in diseases where scarring is the basic pathogenetic mechanism would be immense. Rather than to list the results and conflicting data of numerous studies, this article hopes to provide a general overview of the recent developments.
Animal ; Cell Adhesion Molecules/physiology ; Collagen/physiology ; Extracellular Matrix/physiology ; Fetus/*physiology ; Growth Substances/physiology ; Human ; *Wound Healing

The process of human embryo implantation is mediated not only by evolutionarily conserved mechanisms, but also by a mechanism unique to humans. Evidence suggests that the cell adhesion molecules, L-selectin and trophinin, play a unique role in human embryo implantation. Here, we describe the dual roles of mucin carbohydrate ligand for L-selectin and trophinin protein and of the trophinin-associated proteins bystin and tastin. We then describe trophinin-mediated signal transduction in trophectoderm cells and endometrial epithelial cells. This review also covers cadherin and integrin in human embryo implantation.
Cadherins ; physiology ; Cell Adhesion Molecules ; physiology ; Embryo Implantation ; Epithelial Cells ; metabolism ; Humans ; Integrins ; physiology ; L-Selectin ; physiology ; Signal Transduction

In order to determine the effect of ultraviolet radiation (UVR) on the cell adhesion molecules expressed in human dermal microvascular endothelial cells (HDMEC), the cells were exposed to varying UVR doses and the cell surface was examined for expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM- 1), and E-selectin. The effect of UVB irradiation on the binding of T lymphocytes to HDMEC was also examined. UVA irradiation did not affect the surface expression of ICAM-1, VCAM-1, or E-selectin on the HDMEC. However, following UVB exposure, ELISA demonstrated a significant increase in the baseline ICAM-1 cell surface expression on the HDMEC. However, no induction of either E-selectin or VCAM-1 was noted. UVB also significantly augmented ICAM-1 induction by IL-1 alpha and TNF- alpha. VCAM-1 was induced by stimulating HDMEC with IL-1alpha following a UVB irradiation dose of 100 mJ/cm2. Flow cytometric analysis of the HDMEC stimulated with IL-1 alpha for 24h demonstrated that 12% of the cells expressed VCAM-1 but either IL-1 alpha or UVB irradiation alone failed to induce VCAM-1 expression. Enhancement of T cell-HDMEC binding by IL-1 alpha; or TNF- alpha treatment was not significantly affected after UVB irradiation. This study demonstrated that UVB irradiation can alter ICAM-1 and VCAM-1 expression on the HDMEC surface and that augmentation of ICAM-1 expression and the IL-1 alpha -dependent induction of VCAM-1 following UVB exposure might be important steps in the pathogenesis of sunburn.
Cell Adhesion/radiation effects ; Cell Adhesion Molecules/*metabolism ; Cells, Cultured ; Endothelium, Vascular/cytology/*physiology ; Human ; Microcirculation ; Skin/*blood supply ; T-Lymphocytes/*physiology ; *Ultraviolet Rays

Altitude ; Animals ; CA1 Region, Hippocampal ; metabolism ; physiology ; Male ; Neural Cell Adhesion Molecules ; metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors

Neuroligins (NLs) are postsynaptic membrane proteins expressed in the brain and mediate synaptogenesis. Neuroligin family proteins can specifically induce either excitatory or inhibitory synapses. Deletions or point mutations in neuroligin genes are found in patients with autism spectrum disorders (ASD) or mental retardations. The dysfunctions of these mutations have been tested in multiple neuroligin mouse models. In most of the models, including the human autism-linked NL3 and NL4 mutation mice, there are social interaction defects, memory impairment and repetitive behaviors. Researchers also found the excitatory/inhibitory synapse ratio altered in those mice, as well as receptor subunit composition. However, inconsistencies and debates also exist between different research approaches. In this review, we summarize the neuroligin mouse models currently available, examine the detailed alterations detected in those mice and compare the differences within different mouse models or different investigation methods, to obtain an overall picture of the current progress on neuroligin mouse models.
Animals ; Autistic Disorder ; physiopathology ; Brain ; physiopathology ; Cell Adhesion Molecules, Neuronal ; physiology ; Disease Models, Animal ; Humans ; Membrane Proteins ; physiology ; Mice ; Mutation ; Nerve Tissue Proteins ; physiology ; Synapses ; physiology

OBJECTIVETo study the roles of stromal interaction molecule 2 (STIM2) and transient receptor potential canonical 3 (TRPC3) in extracellular Ca(2+)-sensing receptor (CaR)-induced extracellular Ca2+ influx and the production of nitric oxide (NO) in human umbilical vein endothelial cells (HUVEC).

METHODS(1) The interaction of STIM2 and TRPC3 was determined using the immunofluorescence technique. (2) The expressions of STIM2 and TRPC3 genes were silenced in HUVEC by transfection constructed STIM2 and TRPC3 RNA interference plasmids. The interference efficiency of STIM2, TRPC3 protein and mRNA levels were determined by Western blot and real time RT-PCR, respectively. (3) The second to fifth passage of HUVEC were divided into: STIM2-002 short hairpin RNA (STIM2-002 shRNA ) + spermine + Ca2+ group and TRPC3-004 short hairpin RNA (TRPC3-004 shRNA ) + spermine + Ca2+ group; control group (spermine + Ca2+ group) and vehicle+ spermine + Ca2+ group. The four groups of cells were incubated with CaR agonist spermine, the intracellular Ca2+ concentration ([Ca2+]i) was detected using the fluorescence Ca2+ indicator Fura-2/AM, and the production of NO was determined by DAF-FM (NO fluorescent probe) of each group in HUVEC.

RESULTS(1) Immunofluorescence technique results showed that STIM2 and TRPC3 proteinswere present in the cytoplasm of HUVEC. (2) The results of transfection constructed STIM2 and TRPC3 RNA interference plasmids demonstrated that shRNA targeted to the STIM2 and TRPC3 genes decreased STIM2 and TRPC3 mRNA levels by 88.2% and 74.0%, respectively (P < 0.05), simultaneously, the STIM2 and TRPC3 protein levels were decreased by 79.9% and 71.8%, respectively (P < 0.05). (3) Compared with spermine + Ca2+ group, the [Ca2+]i and the net NO fluorescence intensity of spermine + Ca(2+) + ShSTIM2-002 group, spermine + Ca(2+) + ShTRPC3-004 group and spermine + Ca2+ Vehicle group were not changed (P > 0.05).

CONCLUSIONSTIM2 and TRPC3 do not participate in CaR-mediated Ca2+ influx and NO production individually.

Calcium ; metabolism ; Cell Adhesion Molecules ; physiology ; Cells, Cultured ; Human Umbilical Vein Endothelial Cells ; physiology ; Humans ; Nitric Oxide ; metabolism ; Stromal Interaction Molecule 2 ; TRPC Cation Channels ; physiology

The interactions between blood cells and blood cells or blood cells and endothelium of blood vessel are mainly mediated by adhesion molecules. The role of adhesion molecules is diverse in vivo, which involved in adhesion, migration, differentiation and signal transduction of blood cells. The function of adhesion molecules is necessary to maintain the normal structure and fulfill many physiological processes of these cells. Therefore, the abnormal or deficiency of their expression and function will disrupts normal physiological processes and results in clinical disease. In this paper, several generic classes of adhesion molecules, including the integrins, the selectins, the immunoglobulin superfamily and others are introduced, and a lot of related physiopathological status, such as inflammation, hemostasis, arteriosclerosis, thrombosis and stem cell homing are discussed. The studies on the adhesion molecules of blood cells will contribute not only to understand the pathogenesis of some disorders, but also to search new targets in diagnosis and treatment of these diseases.
Animals ; Antibodies, Monoclonal ; therapeutic use ; Arteriosclerosis ; etiology ; Blood Cells ; chemistry ; Cell Adhesion Molecules ; antagonists & inhibitors ; physiology ; Humans ; Inflammation ; etiology ; Integrins ; physiology ; Selectins ; physiology ; Thrombosis ; etiology

OBJECTIVETo review the recent developments in and research into binding receptors of hepatitis C virus (HCV) and especially the role of dendritic cell-specific adhesion receptor (DC-SIGN) in HCV.

DATA SOURCESBoth Chinese- and English-language literature was searched using MEDLINE (2000 - 2003) and the databank of Chinese-language literature (2000 - 2003).

STUDY SELECTIONRelevant articles on DC-SIGN and HCV binding receptors in recent domestic and foreign literature were selected.

DATA EXTRACTIONData were mainly extracted from 40 articles which are listed in the references section of this review.

RESULTSDC-SIGN, a dendritic cell-specific adhesion receptor and a type II transmembrane mannose-binding C-type lectin, is very important in the function of dendritic cells (DC), both in mediating naïve T cell interactions through ICAM-3 and as a rolling receptor that mediates the DC-specific ICAM-2-dependent migration processes. It can be used by HCV and other viral and bacterial pathogens including human immunodeficiency virus (HIV), Ebola virus, CMV and Mycobacterium tuberculosis to facilitate infection. Both DC-SIGN and DC-SIGNR can act either in cis, by concentrating virus on target cells, or in trans, by transmission of bound virus to a target cell expressing appropriate entry receptors. Recent report showed that DC-SIGN not only plays a role in entry into DC, HCV E2 interaction with DC-SIGN might also be detrimental to the interaction of DC with T cells during antigen presentation.

CONCLUSIONSDC-SIGNs are high-affinity binding receptors for HCV. The clinical strategies that target DC-SIGN may be successful in restricting HCV dissemination and pathogenesis as well as directing the migration of DCs to manipulate appropriate immune responses in autoimmunity and tumorigenic situations.

Animals ; Cell Adhesion Molecules ; physiology ; Gene Products, nef ; physiology ; Hepacivirus ; physiology ; Humans ; Lectins, C-Type ; physiology ; Receptors, CCR5 ; physiology ; Receptors, Cell Surface ; physiology ; Receptors, Virus ; physiology ; Viral Envelope Proteins ; physiology