| Gene name: | LMNB1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HBEC |
| Gene ID: | 4001 |
| Category: | protein coding |
| Phenotype: | Chronic obstructive pulmonary disease |
| Experimental category: | L |
| PMID: | 30692212 |
| Experiment: | SA-β-gal activity assay//Knockdown//Immunostaining//ELISA//Western blot |
| Description: | Lamin B1 knockdown was sufficient to induce cellular senescence by means of SA-β-gal staining, phospho-histone H2A.X (Ser139) staining of DNA damage, and Western blotting of CDKN2A/p16 and CDKN1A/p21, which was significantly enhanced by CSE treatment in HBEC. To determine SASP status, CXCL8 secretion was examined. Significant increase in CXCL8 secretion was observed in conditioned medium only from CSEtreated HBEC with lamin B1 knockdown, indicating that both CSE and lamin B1 reduction to some extent are necessary for progression to full senescence with SASP. |
| Regulatory pathway: | MTOR |
| R-AG-Pathway: | Downregulation |
| Official symbol(s): | MTOR |
| Pathway experiment: | Western blot//Knockdown//qRT-PCR |
| Pathway description: | In comparison with non-smoker lungs, electron microscopic evaluations showed a significant increase in mitochondrial counts in airway epithelial cells in COPD lungs . In comparison with nonsmokers and non-COPD smokers, lamin B1 and DEPTOR mRNA were significantly reduced in HBEC of COPD patients. Consistent with CS-exposed mouse models, no apparent reduction of lamin B1 and DEPTOR expression levels and no increase in p-S6K were demonstrated in alveolar lesions in COPD lungs. These results suggest the existence of pathogenic link between reduced lamin B1–mediated MTOR signaling and enhanced mitochondrial accumulation associated with accelerated cellular senescence in airway epithelial cells during COPD development. |
Annotation:
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