Isolated mesophyll cells from Zinnia elegans are induced by auxin and cytokinin to form tracheary elements (TEs) in vitro with high synchrony. To reveal the changing patterns of gene expression during the 48 h of transdifferentiation from mesophyll to TE cell fate, we used a cDNA-amplified fragment length polymorphism approach to generate expression profiles of >30,000 cDNA fragments. Transcriptional changes of 652 cDNA fragments were observed, of which 304 have no previously described function or sequence identity. Sixty-eight genes were upregulated within 30 min of induction and represent key candidates for the processes that underlie the early stages of commitment and differentiation to a TE cell fate.
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http://dx.doi.org/10.1105/tpc.005231 | DOI Listing |
Arterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
J Tissue Eng
January 2025
Department of Spinal Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Rotator cuff tendon injuries often lead to shoulder pain and dysfunction. Traditional treatments such as surgery and physical therapy can provide temporary relief, but it is difficult to achieve complete healing of the tendon, mainly because of the limited repair capacity of the tendon cells. Therefore, it is particularly urgent to explore new treatment methods.
View Article and Find Full Text PDFHeliyon
January 2025
CAS Key Laboratory of Computational Biology, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Feeding disruption is closely linked to numerous diseases, yet the underlying molecular mechanisms remain an important but unresolved issue at the molecular level. We hypothesize that, at the network level, dietary disruptions can alter gene co-expression patterns, leading to an increase in disease-associated modules, and thereby elevating the likelihood of disease occurrence. Here, we investigate this hypothesis using transcriptomic data from a large cohort of adult mice subjected to feeding disruptions.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Oral Histology-Developmental Biology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Republic of Korea.
Our previous studies indicate that NFI-C is essential for tooth root development and endochondral ossification. However, its exact role in calvarial intramembranous bone formation remains unclear. In this study, we demonstrate that the disruption of the gene leads to defects in intramembranous bone formation, characterized by decreased osteogenic proliferative activity and reduced osteoblast differentiation during postnatal osteogenesis.
View Article and Find Full Text PDFFront Oncol
January 2025
Department of Colorectal Hernia Surgery, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Background And Objective: MicroRNAs (miRNAs) are implicated in cancer by exerting roles in tumor growth, metastasis, and even drug resistance. The general trends of miRNA research in diverse cancers are not fully understood. In this work, miRNA-related research in colorectal cancer, prostate cancer, leukemia, and brain tumors was analyzed in search of key research trends with clinical potential.
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