PMID- 37548627
OWN - NLM
STAT- MEDLINE
DCOM- 20230913
LR  - 20231004
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 60
IP  - 3
DP  - 2023 Sep 1
TI  - TREATMENT WITH HUMAN UMBILICAL CORD-DERIVED MESENCHYMAL STEM CELLS IN A PIG MODEL 
      OF SEPSIS-INDUCED ACUTE KIDNEY INJURY: EFFECTS ON MICROVASCULAR ENDOTHELIAL CELLS 
      AND TUBULAR CELLS IN THE KIDNEY.
PG  - 469-477
LID - 10.1097/SHK.0000000000002191 [doi]
AB  - Background: Approximately 50% of patients with sepsis develop acute kidney injury 
      (AKI), which is predictive of poor outcomes, with mortality rates of up to 70%. 
      The endothelium is a major target for treatments aimed at preventing the 
      complications of sepsis. We hypothesized that human umbilical cord-derived 
      mesenchymal stem cells (hUC-MSCs) could attenuate tubular and endothelial injury 
      in a porcine model of sepsis-induced AKI. Methods: Anesthetized pigs were induced 
      to fecal peritonitis, resulting in septic shock, and were randomized to treatment 
      with fluids, vasopressors, and antibiotics (sepsis group; n = 11) or to that same 
      treatment plus infusion of 1 x 10 6 cells/kg of hUC-MSCs (sepsis+MSC group; n = 
      11). Results: At 24 h after sepsis induction, changes in serum creatinine and 
      mean arterial pressure were comparable between the two groups, as was mortality. 
      However, the sepsis+MSC group showed some significant differences in comparison 
      with the sepsis group: lower fractional excretions of sodium and potassium; 
      greater epithelial sodium channel protein expression; and lower protein 
      expression of the Na-K-2Cl cotransporter and aquaporin 2 in the renal medulla. 
      Expression of P-selectin, thrombomodulin, and vascular endothelial growth factor 
      was significantly lower in the sepsis+MSC group than in the sepsis group, whereas 
      that of Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-kappaB) was lower 
      in the former. Conclusion: Treatment with hUC-MSCs seems to protect endothelial 
      and tubular cells in sepsis-induced AKI, possibly via the TLR4/NF-kappaB signaling 
      pathway. Therefore, it might be an effective treatment for sepsis-induced AKI.
CI  - Copyright (c) 2023 by the Shock Society.
FAU - Ramos Maia, Debora Rothstein
AU  - Ramos Maia DR
AD  - Laboratory for Medical Research 8, Anesthesiology Department, Hospital das 
      Clinicas da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, 
      Brazil.
FAU - Otsuki, Denise Aya
AU  - Otsuki DA
AD  - Laboratory for Medical Research 8, Anesthesiology Department, Hospital das 
      Clinicas da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, 
      Brazil.
FAU - Rodrigues, Camila Eleuterio
AU  - Rodrigues CE
AD  - Laboratory for Medical Research 12, Division of Nephrology, Hospital das Clinicas 
      da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil.
FAU - Zboril, Sabrina
AU  - Zboril S
AD  - Laboratory for Medical Research 8, Anesthesiology Department, Hospital das 
      Clinicas da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, 
      Brazil.
FAU - Sanches, Talita Rojas
AU  - Sanches TR
AD  - Laboratory for Medical Research 12, Division of Nephrology, Hospital das Clinicas 
      da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil.
FAU - Neto, Amaro Nunes Duarte
AU  - Neto AND
AD  - Division of Pathology, Hospital das Clinicas da Faculdade de Medicina da 
      Universidade de Sao Paulo, Sao Paulo, Brazil.
FAU - Andrade, Lucia
AU  - Andrade L
AD  - Laboratory for Medical Research 12, Division of Nephrology, Hospital das Clinicas 
      da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil.
FAU - Auler, Jose Otavio Costa Jr
AU  - Auler JOC Jr
AD  - Laboratory for Medical Research 8, Anesthesiology Department, Hospital das 
      Clinicas da Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, 
      Brazil.
LA  - eng
PT  - Journal Article
DEP - 20230729
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (NF-kappa B)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Vascular Endothelial Growth Factor A)
SB  - IM
MH  - Humans
MH  - *Acute Kidney Injury/therapy/chemically induced
MH  - Endothelial Cells/metabolism
MH  - Kidney/metabolism
MH  - *Mesenchymal Stem Cell Transplantation
MH  - *Mesenchymal Stem Cells/metabolism
MH  - NF-kappa B/metabolism
MH  - *Sepsis/complications/therapy/metabolism
MH  - Toll-Like Receptor 4/metabolism
MH  - Umbilical Cord/metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
MH  - Animals
MH  - Swine
COIS- The authors report no conflicts of interest.
EDAT- 2023/08/07 13:09
MHDA- 2023/09/13 06:41
CRDT- 2023/08/07 10:44
PHST- 2023/09/13 06:41 [medline]
PHST- 2023/08/07 13:09 [pubmed]
PHST- 2023/08/07 10:44 [entrez]
AID - 00024382-990000000-00244 [pii]
AID - 10.1097/SHK.0000000000002191 [doi]
PST - ppublish
SO  - Shock. 2023 Sep 1;60(3):469-477. doi: 10.1097/SHK.0000000000002191. Epub 2023 Jul 
      29.