PMID- 27438970
OWN - NLM
STAT- MEDLINE
DCOM- 20180129
LR  - 20180129
IS  - 2175-8239 (Electronic)
IS  - 0101-2800 (Linking)
VI  - 38
IP  - 2
DP  - 2016 Jun
TI  - p-cresol but not p-cresyl sulfate stimulate MCP-1 production via NF-kappaB p65 in 
      human vascular smooth muscle cells.
PG  - 153-60
LID - S0101-28002016000200153 [pii]
LID - 10.5935/0101-2800.20160024 [doi]
AB  - INTRODUCTION: p-cresol (PC) and p-cresyl sulfate (PCS) are responsible for many 
      of the uremia clinical consequences, such as atherosclerosis in Chronic Kidney 
      Disease (CKD) patients. OBJECTIVES: We investigate the in vitro impact of PC and 
      PCS on monocyte chemoattractant protein-1 (MCP-1) expression via NF-kappa B 
      (NF-kappaB) p65 in VSMC. METHODS: PCS was synthesized by PC sulfatation. VSMC were 
      extracted by enzymatic digestion of umbilical cord vein and characterized by 
      immunofluorescence against alpha-actin antibody. The cells were treated with PC and 
      PCS at their normal (n), uremic (u) and maximum uremic concentrations (m). Cell 
      viability was assessed by MTT. MCP-1 expression was investigated by ELISA in 
      cells supernatants after toxins treatment with or without the NF-kappaB p65 
      inhibitor. RESULTS: There was no significant difference in cell viability after 
      toxins treatment for all concentrations tested. There was a significant increase 
      in MCP-1 expression in cells treated with PCu and PCm (p < 0.001) and PCSn, PCSu 
      and PCSm (p < 0.001), compared with the control. When VSMC were treated with the 
      NF-kappaB p65 inhibitor plus PCu and PCm, there was a significant decrease in MCP-1 
      production (p < 0.005). This effect was not observed with PCS. CONCLUSIONS: VSMC 
      are involved in atherosclerosis lesion formation and production of MCP-1, which 
      contributes to the inflammatory response initiation. Our results suggest that PC 
      mediates MCP-1 production in VSMC, probably through NF-kappaB p65 pathway, although 
      we hypothesize that PCS acts through a different subunit pathway since NF-kappaB p65 
      inhibitor was not able to inhibit MCP-1 production.
FAU - Maciel, Rayana Ariane Pereira
AU  - Maciel RA
AD  - Universidade Federal do Parana, Brazil.
FAU - Rempel, Lisienny Campoli Tono
AU  - Rempel LC
AD  - Universidade Federal do Parana, Brazil.
FAU - Bosquetti, Bruna
AU  - Bosquetti B
AD  - Universidade Federal do Parana, Brazil.
FAU - Finco, Alessandra Becker
AU  - Finco AB
AD  - Universidade Federal do Parana, Brazil.
FAU - Pecoits-Filho, Roberto
AU  - Pecoits-Filho R
AD  - Universidade Catolica do Parana, Brazil.
FAU - Souza, Wesley Mauricio de
AU  - Souza WM
AD  - Universidade Federal do Parana, Brazil.
FAU - Stinghen, Andrea Emilia Marques
AU  - Stinghen AE
AD  - Universidade Federal do Parana, Brazil.
LA  - eng
LA  - por
PT  - Journal Article
TT  - p-cresol mas nao p-cresil sulfato estimulam a producao de MCP-1 via NF-kappaB p65 em 
      celulas vasculares musculares lisas humanas.
PL  - Brazil
TA  - J Bras Nefrol
JT  - Jornal brasileiro de nefrologia
JID - 9426946
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cresols)
RN  - 0 (Sulfuric Acid Esters)
RN  - 0 (Transcription Factor RelA)
RN  - 1MXY2UM8NV (4-cresol)
RN  - 56M34ZQY1S (4-cresol sulfate)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/*drug effects
MH  - Cresols/*pharmacology
MH  - Humans
MH  - Muscle, Smooth, Vascular/*cytology/*metabolism
MH  - Sulfuric Acid Esters/*pharmacology
MH  - Transcription Factor RelA/*physiology
EDAT- 2016/07/21 06:00
MHDA- 2018/01/30 06:00
CRDT- 2016/07/21 06:00
PHST- 2015/09/20 00:00 [received]
PHST- 2015/11/11 00:00 [accepted]
PHST- 2016/07/21 06:00 [entrez]
PHST- 2016/07/21 06:00 [pubmed]
PHST- 2018/01/30 06:00 [medline]
AID - S0101-28002016000200153 [pii]
AID - 10.5935/0101-2800.20160024 [doi]
PST - ppublish
SO  - J Bras Nefrol. 2016 Jun;38(2):153-60. doi: 10.5935/0101-2800.20160024.