Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0314719 (dry eye)
 2,625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radiation therapy is the most widely used and effective treatment for orbital tumors, but it causes dry eye due to lacrimal gland damage. Induced pluripotent stem cell-derived conditioned medium (iPSC-CM) has been shown to rescue different types of tissue damage. The present study investigated the mechanism of the potential radioprotective effect of IPS cell-derived conditioned medium (iPSC-CM) on gamma-irradiation-induced lacrimal gland injury (RILI) in experimental mice. In this study, we found that iPSC-CM ameliorated RILI. iPSC-CM markedly decreased radiotherapy induced inflammatory processes, predominantly through suppressing p38/JNK signaling. Further signaling pathway analyses indicated that iPSC-CM could suppress Akt (Protein Kinase B, PKB) phosphorylation. High levels of midkine (MDK) were also found in iPSC-CM and could be involved in lacrimal gland regeneration by promoting cell migration and proliferation. Thus, our study indicates that inhibiting the p38/JNK pathway or increasing the MDK level might be a therapeutic target for radiation-induced lacrimal gland injury.
...
PMID:Improvement of radiotherapy-induced lacrimal gland injury by induced pluripotent stem cell-derived conditioned medium via MDK and inhibition of the p38/JNK pathway. 2531 1

Radiotherapy-induced lacrimal gland injury often causes dry eye. Oxidative stress and local inflammation are the primary consequences of radiotherapy-induced injury. The most recent research shows that the human-specific gene CHRFAM7A plays an important role in inflammation. However, the effect of CHRFAM7A on radiotherapy-induced lacrimal gland injury remains unclear. In this study, humanized mice were successfully generated via the transplantation of human peripheral blood mononuclear cells that expressed human-specific genes. After radiation, the CHRFAM7A gene was highly expressed in the lacrimal glands of humanized mice, in which it protected the function of the lacrimal gland after radiotherapy. CHRFAM7A down-regulated radiotherapy-induced inflammation by suppressing p38/JNK signalling. CHRFAM7A also inhibited oxidative stress in the haematopoietic system after radiotherapy. Further signalling pathway analyses indicated that CHRFAM7A suppressed Akt (protein kinase B, PKB) phosphorylation. CHRFAM7A may therefore be a therapeutic target in radiation-induced lacrimal gland injury.
 ...
PMID:Human-specific CHRFAM7A protects against radiotherapy-induced lacrimal gland injury by inhibiting the p38/JNK signalling pathway and oxidative stress. 3196 70