Heterogeneous Cell Renewal of Pancreas in Mice: [3H]-thymidine Autoradiographic Investigation

Pancreas ◽  
2002 ◽  
Vol 24 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Yasushi Magami ◽  
Takeshi Azuma ◽  
Hideto Inokuchi ◽  
Fuminori Moriyasu ◽  
Keiichi Kawai ◽  
...  
Keyword(s):  
Cell Renewal ◽  
Autoradiographic Investigation

Cell renewal in human epidermis

1965 ◽  
Vol 92 (4) ◽  
pp. 462-468 ◽  
Author(s):  
W. L. Epstein
Keyword(s):  
Human Epidermis ◽  
Cell Renewal

Progestation

1967 ◽  
Vol 56 (3_Suppla) ◽  
pp. S7-S45 ◽  
Keyword(s):  
Tritiated Thymidine ◽  
Succinic Dehydrogenase ◽  
Glandular Epithelium ◽  
Synthetic Activity ◽  
Cell Renewal ◽  
Pulse Labelling ◽  
Uterine Receptivity ◽  
Alkaline Phosphatases ◽  
Monocytic Cells ◽  
Acid And Alkaline Phosphatases

ABSTRACT Autoradiographic, enzymic and histologic studies on uteri of pregnant rats were carried out to follow the endometrial modifications which take place during progestation (days L0 – L4) and culminate in the state of uterine receptivity essential for ovum-implantation. Pulse labelling with tritiated thymidine (radioactive DNA precursor) on L0, L1 and L2 revealed a sequence of cell renewal in luminal and glandular epithelium and endometrial stroma. On L3 and L4 stromal cells showed extensive incorporation of tritiated thymidine. This synthetic activity was associated with endometrial preparation for decidualization and was evoked at least in part, by the surge of oestrogen on L3. All layers of the uterine wall were heavily infiltrated on L0 and resembled the site of an acute inflammatory reaction. Subsequently, polymorphonuclear infiltration diminished and monocytic cells predominated. On L3 a spatial arrangement was observed: eosinophiles were concentrated in the basal endometrium and monocytic cells in the subepithelial stroma. A comparison was made between such a shift in migratory cells in the uterus and similar phenomena which occur in inflammatory and immune reactions. Activities of acid and alkaline phosphatases, of ATP-ase and succinic dehydrogenase were low on L0 and L1 during the periods of infiltration, degeneration and regeneration of luminal and glandular epithelium. Enzymic activities increased on the following days, (L3 and L4). Vascular dilation and engorgement and endometrial oedema were observed near the blastocysts on L4. Most blastocysts incorporated tritiated thymidine after 14.00 h on L4, but some showed uptake before loss of the zona which occurs usually between 14.00 and 16.00 h; therefore, it was assumed that the permeability of the zona increases prior to being shed. Activities of succinic dehydrogenase and acid and alkaline phosphatases were demonstrable in blastocysts on L4 while they were still »free« in the uterine lumen.

CDK12 Promotes Breast Cancer Progression and Maintains Stemness by Activating c-myc/β -catenin Signaling

2020 ◽  
Vol 20 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Fang Peng ◽  
Chuansheng Yang ◽  
Yanan Kong ◽  
Xiaojia Huang ◽  
Yanyu Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Lung Metastasis ◽  
Xenograft Model ◽  
Breast Cancer Cell Lines ◽  
Cell Renewal ◽  
Cancer Stemness ◽  
Mesenchymal Transition ◽  
Potential Biomarker

Background: CDK12 is a promising therapeutic target in breast cancer with an effective ability of maintaining cancer cell stemness. Objective: We aim to investigate the mechanism of CDK12 in maintaining breast cancer stemness. Methods: CDK12 expression level was accessed by using RT-qPCR and IHC. CDK12-altered breast cancer cell lines MDA-MB-231-shCDK12 and SkBr-3-CDK12 were then established. CCK8, colony formation assays, and xenograft model were used to value the effect of CDK12 on tumorigenicity. Transwell assay, mammosphere formation, FACS, and lung metastasis model in vivo were determined. Western blot further characterized the mechanism of CDK12 in breast cancer stemness through the c-myc/β-catenin pathway. Results: Our results showed a higher level of CDK12 exhibited in breast cancer samples. Tumor formation, cancer cell mobility, spheroid forming, and the epithelial-mesenchymal transition will be enhanced in the CDK12high group. In addition, CDK12 was associated with lung metastasis and maintained breast cancer cell stemness. CDK12high cancer cells presented higher tumorigenicity and a population of CD44+ subset compared with CDK12low cells. Our study demonstrated c-myc positively expressed with CDK12. The c-myc/β-catenin signaling was activated by CDK12, which is a potential mechanism to initiate breast cancer stem cell renewal and may serve as a potential biomarker of breast cancer prognosis. Conclusion: CDK12 overexpression promotes breast cancer tumorigenesis and maintains the stemness of breast cancer by activating c-myc/β-catenin signaling. Inhibiting CDK12 expression may become a potential therapy for breast cancer.

scholarly journals Injury-Induced Innate Immune Response During Segment Regeneration of the Earthworm, Eisenia andrei

2021 ◽  
Vol 22 (5) ◽  
pp. 2363
Author(s):  
Kornélia Bodó ◽  
Zoltán Kellermayer ◽  
Zoltán László ◽  
Ákos Boros ◽  
Bohdana Kokhanyuk ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Immune Cell ◽  
Scavenger Receptor ◽  
Cell Renewal ◽  
Body Parts ◽  
Eisenia Andrei ◽  
Blastema Formation ◽  
Close Proximity ◽  
Renewal Period

Regeneration of body parts and their interaction with the immune response is a poorly understood aspect of earthworm biology. Consequently, we aimed to study the mechanisms of innate immunity during regeneration in Eisenia andrei earthworms. In the course of anterior and posterior regeneration, we documented the kinetical aspects of segment restoration by histochemistry. Cell proliferation peaked at two weeks and remitted by four weeks in regenerating earthworms. Apoptotic cells were present throughout the cell renewal period. Distinct immune cell (e.g., coelomocyte) subsets were accumulated in the newly-formed blastema in the close proximity of the apoptotic area. Regenerating earthworms have decreased pattern recognition receptors (PRRs) (e.g., TLR, except for scavenger receptor) and antimicrobial peptides (AMPs) (e.g., lysenin) mRNA patterns compared to intact earthworms. In contrast, at the protein level, mirroring regulation of lysenins became evident. Experimental coelomocyte depletion caused significantly impaired cell divisions and blastema formation during anterior and posterior regeneration. These obtained novel data allow us to gain insight into the intricate interactions of regeneration and invertebrate innate immunity.

scholarly journals GCT-73. EXPRESSION PROFILING OF INTRACRANIAL GERM CELL TUMORS REVEALS UPREGULATION OF RAS THROUGH mRNA-microRNA SIGNALING PATHWAY

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii343-iii343
Author(s):  
Aaron M Taylor ◽  
Jianhe Shen ◽  
Lingzhao Ren ◽  
Keita Terashima ◽  
Lei Huang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Germ Cell ◽  
Expression Profiling ◽  
Model Building ◽  
Rna Binding ◽  
Molecular Subtype ◽  
Germ Cell Tumors ◽  
Cell Renewal ◽  
Data Set ◽  
Intracranial Germ Cell Tumors

Abstract Intracranial germ cell tumors (IGCTs) account for 3% of CNS tumors in children in the U.S. and 11% in Japan and East Asian countries. IGCTs are separated into two distinct subtypes based on histology: germinomas and non-germinomatous germ cell tumors (NGGCTs). The deep central location of IGCTs makes surgical resection and therefore molecular subtype classification difficult, and previous gene expression studies are limited. We performed mRNA expression profiling (Human Genome U133 Plus 2.0) and microRNA expression profiling (ABI TaqMan) with 36 and 49 IGCTs, respectively. Sample stratification using non-negative matrix factorization clustering of gene expression revealed two distinct subgroups that delineated germinomas from NGGCTs. Employing stepwise model building in each data set separately, we were able to separate these groups using only mRNA probes for the LIN28B and L1TD1 genes, and two microRNA, microRNA-26a and microRNA-373. MicroRNA26a suppresses the LIN28B gene and is down-regulated in germinoma. LIN28B directly binds and suppresses the let-7 microRNA family, which suppress the KRAS oncogene, previously found to be mutated in ~19% of IGCTs. L1TD1 is required for human stem cell renewal and directly interacts with LIN28B for its RNA binding function. LIN28B and L1TD1 are both known to be upregulated in other systemic germ cell tumors, but this has not yet been documented in IGCTs. In conclusion, these results show that intracranial germinomas have similar gene expression compared to systemic seminoma, and suggest a mechanism by which activation of LIN28B and L1TD1 downregulates the let-7 microRNA and subsequently upregulates KRAS.

Multi-omics approach to post-CABG renal impairment

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Boerschel ◽  
B Geelhoed ◽  
L Conradi ◽  
E Girdauskas ◽  
C Mueller ◽  
...  
Keyword(s):  
Renal Impairment ◽  
Leucine Zipper ◽  
Mixed Model ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Control Cell ◽  
Integrated Approach ◽  
Cell Renewal ◽  
Gene Expressions ◽  
Tissue Samples

Abstract Background Renal impairment is a common complication after CABG (coronary artery bypass graft) surgery associated with an adverse outcome. Purpose To further characterize the molecular framework of the disease through omics analyses. Methods In N=165 CABG patients we performed multi-omics-analyses in preoperatively collected blood and tissue samples as well as 991 creatinine measurements. We used multivariable mixed-model regression analyses to analyse post-operative creatinine increase and to find common genetic polymorphisms, transcripts, metabolites and/or proteins associated with changes in postoperative creatinine increase. Multiple testing was accounted for by setting a 5%-limit on the false discovery rate (FDR) using the Benjamini-Hochberg procedure. Results Post-operative increase of log transformed creatinine was 0.035 (8%); 95% confidence interval (CI) 0.025, 0.045; P<0.001. We identified 55 gene expressions and two proteins associated with post-CABG renal impairment. On the metabolomic and single nucleotide point mutation (SNP) level, no relevant targets were found. The three most important identified gene expressions were MIR3202.1 (beta of log transformed creatinine increase per standard deviation gene expression increase −0.034; 95% CI: −0.048, 0.020; P<0.001), LOC105374386 (−0.032; 95% CI: −0.046, 0.019; P<0.001) and maternal embryonic leucine zipper kinase (MELK) (−0.022; 95% CI: −0.032, 0.013; P<0.001). Expression of all three was associated with a lower risk of post-CABG renal impairment. The same applies to the identified protein CAPRIN2 (−0.042; 95% CI: −0.062, 0.022; P<0.001), while expression of the protein TUBB6 was associated with a higher risk (0.033; 95% CI: 0.017, 0.048; P<0.001). Conclusions In an integrated approach we identified omics-biomarkers for the prediction of renal impairment after CABG surgery. The underlying pathophysiological associations of these genes and proteins are not fully understood. MELK might be an interesting target for further investigations, as it plays a prominent role in cell cycle control, cell proliferation, apoptosis, cell migration and cell renewal. Our results may help to better identify individuals at risk and lay the methodological groundwork for further omics analyses. Funding Acknowledgement Type of funding source: None

Effect of lumenal contents on colonic cell replacement.

1977 ◽  
Vol 233 (3) ◽  
pp. E208
Author(s):  
J Stragand ◽  
R F Hagemann
Keyword(s):  
Cell Renewal ◽  
Physical Stimulation ◽  
Nutritional Factors ◽  
Cell Replacement ◽  
Cell Production ◽  
Physiological Capacity ◽  
Fasting And Refeeding

Recent studies have shown that the rate of colonic cell renewal can be altered through fasting and refeeding, which produces a marked depression and transient stimulation, respectively. In the present study, the role of physical versus nutritional stimulation in the colonic fasting-refeeding response and the renewal of the functional colonic compartment were evaluated via a nondestructive colonic ligation procedure. The results reported herein suggest that physical stimulation by lumenal factors is in part required to initiate the colonic hyperplasia seen after refeeding. Blood-borne nutritional factors, in the absence of physical stimulation, cannot alone stimulate colonic cell production. Additional evidence is presented which suggests that this physical stimulation may be manifested through the lumenal distension produced by the newly ingested food materials. The results are discussed from the viewpoint of influencing the functional colonic compartment and physiological capacity.

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