Low back pain (LBP) is one of the most prevalent conditions which need medical advice and result in chronic disabilities. Degenerative disc disease (DDD) is a common reason for LBP. A lot of researchers think that CEP degeneration play critical roles in the initiation and development of DDD. In recent years, researchers have put interests on cell-based therapies for regenerating disc structure and function. Our research team has isolated cartilage endplate-derived stem cells (CESCs) and validated their chondrogenic and osteogenic differentiation ability. Enhanced chondrogenic differentiation and inhibited osteogenic differentiation of CESCs may retard CEP calcification and restore the nutrition supply, possibly regenerating the degenerated discs.
Global Gene Expression Profiling and Alternative Splicing Events during the Chondrogenic Differentiation of Human Cartilage Endplate-Derived Stem Cells.
Specimen part
View SamplesWe did microarray experiments to elucidate the transcriptome changes due to TCF-1 deficiency in Tfh cells. These data clearly demonstrate that Tfh-associated genes were down-regulated in TCF-1-null Tfh cells, whereas Th1-associated signatures were up-regulated, indicating that TCF-1 initiates the Tfh fate by directly strengthening Tfh signatures while suppressing Th1-associated genes.
The transcription factor TCF-1 initiates the differentiation of T(FH) cells during acute viral infection.
Specimen part
View SamplesMicroarray experiments were performed to elucidate the transcriptome changes due to EZH2 deficiency in follicular T helper (TFH) cells. These data suggest TFH-lineage associated genes are down-regulated in EZH2-null TFH cells, indicating that EZH2 primes TFH differentiation by regulating canonical genes of TFH cells.
The histone methyltransferase EZH2 primes the early differentiation of follicular helper T cells during acute viral infection.
Specimen part, Time
View SamplesFollicular regulatory T (Tfr) cells maintain homeostasis of humoral immunity by suppressing germinal center responses. TFR cells are differentiated from conventional regulatory T (Treg) cells, but underlying mechanisms remain largely unknown.
No associated publication
Specimen part
View SamplesLong term-exposed to high altitude, the increased numbers of red blood cells tend to stabilize to a certain extend in most people, but someone will occur over-increasing in number of red blood cells, which cause a serious of clinical symptoms and signs, and this is high altitude polycythemia. EPO-EPOR system may be the main reasons for erythroid progenitor cell proliferation and differentiation in early exposion to plateau, but, in the late, there may be other factors involved in the regulation of erythropoiesis in bone marrow, multiple factors working together lead to excessive red blood cell proliferation.
No associated publication
Sex, Specimen part, Disease, Disease stage
View SamplesThe expression level of miR-608 was found to be down regulated in several types of cancer. In our previous study, a single SNP in miR-608 (rs4919510) was found to be strongly associated with a higher risk of developing sepsis and multiple organ dysfunctions in all 3 independent study cohorts. However, the clinicopathological impact and the exact roles of miR-608 and its underlying molecular mechanisms in inflammation remain to be identified.
No associated publication
Cell line
View SamplesIn our study, we found the expression of the novel long coding RNA (AP000770.1-1) was positively associated with cholesterol levels in human samples and HepG2 cells.
No associated publication
Specimen part, Cell line
View SamplesCartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could inhibit the osteogenic differentiation of CESCs.
No associated publication
Specimen part
View SamplesETX treatment promoted cardiomyocyte proliferation. To investigate the molecular mechanism, we performed microarray analysis to explore the molecular mechanism underlying the effect of ETX on cardiomyocyte proliferation.
No associated publication
Specimen part, Treatment
View SamplesCaco-2 cells were infected with F. nucleatum (MOI=100:1) or non-infected (control) for 24 hours. Total RNA of cells was extracted using the TRIzol Reagent (Life Technologies) and cDNA was generated using the PimeScript TMRT Reagent Kit (Takara).
TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo.
Specimen part, Cell line
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