Table 1.
Changes in plasma gelsolin concentration in selected diseases evaluated using human samples and suggested mechanisms of pGSN concentration changes.
Disease | pGSN | Material | Detection Method | Suggested Mechanism of pGSN Changes | Ref. | |
---|---|---|---|---|---|---|
Trauma | Major trauma | ↓ | blood | western blot | binding of actin from damaged cells, formation of actin-gelsolin complexes | [18] |
Critically ill patients | ↓ | blood | nucleation assay | binding of actin from damaged cells, formation of actin-gelsolin complexes | [46] | |
Burns | ↓ | blood | ELISA | binding of actin from damaged cells, formation of actin-gelsolin complexes, binding of inflammatory mediators, proteolytic cleavage by MMPs (*) | [12,47,48] | |
Traumatic brain injury | ↓ | blood | ELISA | actin binding, formation of actin-gelsolin complexes, binding of inflammatory mediators and diminishing of neuroinflammation | [50] | |
CPB-ALI | ↓ | blood | ELISA | actin binding, formation of actin-gelsolin complexes, binding of inflammatory mediators | [51] | |
Acute liver injury | ↓ | blood | ELISA | binding of actin released from injured liver | [53] | |
Infections and infectious-associated diseases | Sepsis | ↓ | blood | ELISA, nucleation assay | binding of actin from damaged cells, formation of actin-gelsolin complexes, binding of inflammatory mediators | [17,54,55] |
Malaria | ↓ | blood | nucleation assay, severing assay, western blot, LC/MS/MS | binding of actin released from destroyed erythrocytes, binding of hemozoin and formation of hemozoin-gelsolin complexes | [56,57] | |
HBV-induced cirrhosis | ↓ | blood | 2-DE, MS/MS | not defined | [58] | |
HAD | ↓ | CSF | 2-DE, 2-D DIGE, western blot | not defined | [59] | |
↑ | blood | SELDI-TOF | not defined | [60] | ||
Chronic inflammatory diseases | Rheumatic arthritis | ↓ | blood, synovial fluid | nucleation assay | distribution of gelsolin into inflamed synovial joint space, binding of actin from damaged cells, formation of actin-gelsolin complexes, decreased production (*), proteolytic degradation (*), binding to plasma factors (*) | [61] |
↓ | urine | CE-MS | not defined | [62] | ||
↑ | urine | ELISA | not defined | [63] | ||
Atopic dermatitis | ↓ | blood | ELISA | binding of inflammatory mediators, prevention of Fas-induced keratinocyte apoptosis (*) | [64] | |
Neurological disorders | Alzheimer’s disease | ↓ | CSF | 2-D DIGE, MS, ELISA | not defined | [65] |
TBE, LNB | ↓ | blood | western blot | binding of actin from damaged cells, formation of actin-gelsolin complexes, binding of inflammatory mediators | [66] | |
Multiple sclerosis | ↓ | blood, CSF | western blot | binding of actin from damaged cells, binding of inflammatory mediators and diminishing of neuroinflammation | [67] | |
SAH | ↓ | blood, CSF | ELISA, western blot | proteolytical cleavage by MMP-3, MMP-1 and MMP-9 | [68,69,70] | |
Cancers | Colon cancer | ↑ | blood | ELISA, western blot | interaction with extracellular environment proteins, increase of colon cancer motility | [71] |
Pancreatic cancer and pancreatitis | ↑ | blood | SRM, ELISA | not defined | [72] | |
Breast cancer | ↓ | blood | LC-MS/MS, western blot | BRCA1-dependent recruiting of ATF-1 | [73] | |
Astrocytoma | ↓ | CSF | 2-DE, MALDI-TOF/TOFMS | cleavage by caspase activity | [74] | |
Other diseases | Chronic kidney disease | ↓ | blood | nucleation assay | impaired pGSN synthesis due to muscle wasting, actin-mediated increase of gelsolin clearance | [75] |
AAC | ↓ | blood | ELISA | not defined | [76] | |
Diabetes | ↓ | blood | LC-MS | binding of actin from damaged cells, formation of actin-gelsolin complexes, protein anabolism | [77] | |
Diabetic retinopathy | ↓ | blood | SQ-MRM, SID-MRM | not defined | [78] | |
Pre-eclampsia | ↓ | blood | ELISA | binding of actin from damaged cells, formation of actin-gelsolin complexes, proteolytic cleavage by MMPs | [79,80] | |
Rhabdomyolysis | ↑ | blood | radioimmunoassay | induced synthesis, liberation of GSN from gelsolin-actin complexes | [81] | |
FAF | ↑ | blood | nucleation assay | impaired gelsolin-actin interactions resulting from mutation in pGSN | [82] |
Abbreviations: ELISA: enzyme linked immunosorbent assay; CPB-ALI: acute lung injury (ALI) induced by cardiopulmonary bypass; LC/MS/MS: liquid chromatography-mass spectrometry; 2-DE: two-dimensional electrophoresis; MS/MS: mass spectrometry analysis; HAD: HIV1-associated dementia; CSF: cerebrospinal fluid; 2-D DIGE: 2-DE difference gel electrophoresis; SELDI-TOF: surface-enhanced laser desorption/ionization time-of-flight; TBE: tick-borne encephalitis; LNB: Lyme neuroborreliosis; SRM: selected reaction monitoring; SAH: subarachnoid hemorrhage; CE-MS: capillary electrophoresis-mass spectrometry; MALDI-TOF: matrix-assisted laser desorption ionization-time of flight; AAC: aortic arch calcification; SQ-MRM: semiquantitative multiple reaction monitoring; SID-MRM: stable-isotope dilution multiple reaction monitoring; FAF: familial amyloidosis of Finnish type; (*) potential mechanism, not confirmed during the course of the study.