Immature multipotent embryonic peripheral glial cells, the Schwann cell precursors (SCPs), differentiate into melanocytes, parasympathetic neurons, chromaffin cells, and dental mesenchymal populations. Here, genetic lineage tracing revealed that, during murine embryonic development, some SCPs detach from nerve fibers to become mesenchymal cells, which differentiate further into chondrocytes and mature osteocytes. This occurred only during embryonic development, producing numerous craniofacial and trunk skeletal elements, without contributing to development of the appendicular skeleton. Formation of chondrocytes from SCPs also occurred in zebrafish, indicating evolutionary conservation. Our findings reveal multipotency of SCPs, providing a developmental link between the nervous system and skeleton.
The efficacy of TELD is relatively good for the selected young and elderly patients in this study. Therefore, age is not a predictor of TELD surgery-related outcomes.
Abstract. Recent studies have suggested that the RAS protein activator like-1 (RASAL1) is a potential tumor suppressor, which is found to be reduced in certain human cancers. Its downregulation is involved in the progression of malignancies. However, whether or not RASAL1 plays a role in the development of gastric cancer remains to be determined. Our study aimed to clarify the role of RASAL1 in the progression of gastric adenocarcinoma. The expression of RASAL1 in primary gastric adenocarcinoma tissue specimens was determined by immunohistochemistry. The expression of RASAL1 mRNA and protein was detected by RT-PCR and western blotting in gastric adenocarcinoma cell lines with varying differentiation statuses, including well-differentiated MKN-28, moderately differentiated SGC-7901 and poorly differentiated BGC-823, respectively. A normal gastric epithelial cell line, GES-l, was used as the control line. The immunohistochemical results revealed that the expression of the RASAL1 protein was mainly observed in the cytoplasm. Among 50 cases of gastric adenocarcinoma tissues, 12 cases were identified as (-), 23 cases (+), 13 cases (++) and 2 cases (+++). Among 50 cases of normal gastric tissues, 16 cases were (++) and 34 cases (+++). The expression of the RASAL1 protein was found to be decreased in the gastric adenocarcinoma tissue compared with normal gastric tissue (p<0.01). Moreover, in the gastric carcinoma tissues, the expression of RASAL1 was correlated with carcinoma diameter, differentiation grades, invasive depth, lymph node metastasis and TNM. Additionally, the RASAL1 mRNA and proteins were decreased in the three gastric adenocarcinoma cell lines compared with the normal gastric epithelial cell line GES-l. In addition, the downregulation of RASAL1 correlated with the differentiation status of cancer cell lines. Based on the above investigation, we conclude that expression of the RASAL1 gene is decreased in gastric carcinoma tissues and cell lines. The results indicate that RASAL1 may be important in the tumorigenesis and development of gastric carcinoma.
The dorsal horn (DH) of the spinal cord is the integrative center that processes and transmits pain sensation. Abnormal changes in ion channel expression can enhance the excitability of pain-related DH neurons. Sodium-activated potassium (KNa) channels are highly expressed particularly in the central nervous system; however, information about whether rat DH neurons express the SLICK channel protein is lacking, and the direct effects on SLICK in response to inflammation and the potential signaling pathway mediating such effects are yet to be elucidated. Here, using cultured DH neurons, we have shown that tumor necrosis factor-α inhibits the total outward potassium current IK and the KNa current predominantly as well as induces a progressive loss of firing accommodation. However, we found that this change in channel activity is offset by the p38 inhibitor SB202190, thereby suggesting the modulation of SLICK channel activity via the p38 MAPK pathway. Furthermore, we have demonstrated that the tumor necrosis factor-α modulation of KNa channels does not occur at the level of SLICK channel gating but arises from possible posttranslational modification.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.