Results
| PMID | 21333981 |
| Gene Name | HSPA4 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 38 |
| Population details | 38 (18 with endometriosis, 20 without endometriosis) |
| Sex | Female |
| Associated genes | HSP70 |
| Other associated phenotypes |
Endometriosis |
|
Fertil Steril. 2011 Apr;95(5):1560-7.e1-3. doi: 10.1016/j.fertnstert.2011.01.122. Chehna-Patel, Nina| Warty, Neeta| Sachdeva, Geetanjali| Khole, Vrinda Department of Gamete Immunobiology, National Institute for Research in Reproductive Health, Indian Council of Medical Research, Parel, Mumbai, India. OBJECTIVE: To investigate the mechanism underlying the appearance of a 20-kd HSP70 fragment and its consequences in the ectopic endometrium of endometriosis patients. DESIGN: Experimental study. SETTING: Research institute and obstetrics and gynecology clinic. PATIENT(S): Participants with (n = 18) and without (n = 20) endometriosis. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Reverse-transcription polymerase chain reaction, protease assays, and in silico tools were used to investigate the origin of the 20-kd HSP70 fragment. Immunocolocalization studies were carried out to determine whether subtilisin/kexin isozyme 1 (SKI-1) and HSP70 are colocalized. Expression and localization of surrogate markers of inflammation, such as nuclear factor NF-kappaB and interleukin IL-6 were examined by immunoblotting and in situ studies. RESULT(S): HSP70 is posttranslationally processed into a 20-kd fragment by SKI-1, a protease of the subtilisin family, in ectopic endometrium (ECE). Immunocolocalization studies revealed spatial proximity of SKI-1 and HSP70 in ECE. Furthermore, ECE demonstrated nuclear localization of the transcription factor, NF-kappaB and high expression of its target protein, IL-6. CONCLUSION(S): This study hints at the possible mechanisms underlying the trimming of HSP70 in ECE and also at the role of proteases in the pathogenesis of endometriosis. The possible repercussions of HSP70 fragmentation include dysregulation of key regulatory proteins, resulting in the escalation of inflammatory events in endometriotic lesions. Mesh Terms: Adult| Base Sequence| Endometriosis/*etiology/genetics/metabolism/pathology| Female| HSP70 Heat-Shock Proteins/genetics/*metabolism| Humans| Molecular Sequence Data| Peritoneal Diseases/*etiology/genetics/metabolism/pathology| Proprotein Convertas |
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