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Background
Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to the human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.
Results
In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the PM2.5 group and FA group during the period of PM2.5 exposure. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure resulted in the activation of the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, P62 and beclin-1 activated. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure.
Conclusions
Taken together, our findings indicated that PM2.5-induced renal injury via the activation of the autophagic pathway in renal tubular epithelial cells.
Keywords
PM2.5, Renal injury, Autophagic pathway
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CURRENT STATUS: Published
View the published article at Environmental Sciences Europe.
No community comments so far
Editorial decision: Accept
On 07 Jul, 2020
Editor assigned
On 07 Jul, 2020
Submission checks complete
On 06 Jul, 2020
Editor invited
On 06 Jul, 2020
Version 1
Posted 27 Apr, 2020
No comments provided
Editorial decision: Minor Revision
On 21 Jun, 2020
Review #4 received
Received 17 Jun, 2020
Review #3 received
Received 09 Jun, 2020
Review #2 received
Received 28 May, 2020
Review #1 received
Received 25 May, 2020
Reviewer #4 agreed
On 18 May, 2020
Reviewer #3 agreed
On 14 May, 2020
Reviewer #2 agreed
On 12 May, 2020
Reviewers invited
Invitations sent on 11 May, 2020
Reviewer #1 agreed
On 11 May, 2020
Editor assigned
On 07 May, 2020
Editor invited
On 06 May, 2020
Submission checks complete
On 22 Apr, 2020
First submitted
On 18 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
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A new preprint design is coming!
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See the published version of this preprint at Environmental Sciences Europe.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Environmental Sciences Europe.
No community comments so far
Editorial decision: Accept
On 07 Jul, 2020
Editor assigned
On 07 Jul, 2020
Submission checks complete
On 06 Jul, 2020
Editor invited
On 06 Jul, 2020
Version 1
Posted 27 Apr, 2020
No comments provided
Editorial decision: Minor Revision
On 21 Jun, 2020
Review #4 received
Received 17 Jun, 2020
Review #3 received
Received 09 Jun, 2020
Review #2 received
Received 28 May, 2020
Review #1 received
Received 25 May, 2020
Reviewer #4 agreed
On 18 May, 2020
Reviewer #3 agreed
On 14 May, 2020
Reviewer #2 agreed
On 12 May, 2020
Reviewers invited
Invitations sent on 11 May, 2020
Reviewer #1 agreed
On 11 May, 2020
Editor assigned
On 07 May, 2020
Editor invited
On 06 May, 2020
Submission checks complete
On 22 Apr, 2020
First submitted
On 18 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Environmental Sciences Europe.
Background
Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to the human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.
Results
In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the PM2.5 group and FA group during the period of PM2.5 exposure. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure resulted in the activation of the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, P62 and beclin-1 activated. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure.
Conclusions
Taken together, our findings indicated that PM2.5-induced renal injury via the activation of the autophagic pathway in renal tubular epithelial cells.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
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