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Research
Elizabeth Vargis
Utah State University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3141-9317
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Background Choroidal neovascularization (CNV) is a major cause of blindness in patients with age-related macular degeneration. CNV is characterized by new blood vessel growth and subretinal fluid accumulation, which results in mechanical pressure on retinal pigment epithelial (RPE) cells. Overexpressing RPE-derived angiogenic factors plays an important role in inducing CNV.
Results The goal of this study was to determine whether low levels of acute mechanical stress during early CNV can induce the expression of angiogenic factors in RPE cells and accelerate angiogenesis. Using a novel device, acute mechanical stress was applied to primary porcine RPE cells and the resulting changes in the expression of major angiogenic factors were examined using immunocytochemistry, qRT-PCR, and ELISA. An in vitro tube formation assay was used to determine the effect of mechanical stress on RPE cells on angiogenesis. Our results showed an increase in the expression of major angiogenic factors in response to mechanical stress, resulting in increased in vitro angiogenesis. Abnormal epithelial-mesenchymal transition (EMT) in RPE cells is also associated with CNV and further retinal degeneration. Our qRT-PCR results verified an increase in the expression of EMT genes in RPE cells.
Conclusions In conclusion, we showed that acute mechanical stress induces the expression of major angiogenic and EMT factors and promotes in vitro angiogenesis, suggesting that mechanical stress plays a role in promoting aberrant angiogenesis in AMD.
Keywords
Mechanical stress, Angiogenesis, RPE, AMD, EMT, CNV, VEGF, IL-6, IL-8, ANG2
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CURRENT STATUS: Published
View the published article at Journal of Biological Engineering.
No community comments so far
Editorial decision: Accept
On 23 Mar, 2020
Review #1 received
Received 20 Mar, 2020
Review #2 received
Received 20 Mar, 2020
Reviewers invited
Invitations sent on 19 Mar, 2020
Reviewer #1 agreed
On 19 Mar, 2020
Reviewer #2 agreed
On 19 Mar, 2020
Editor assigned
On 18 Mar, 2020
Submission checks complete
On 17 Mar, 2020
Editor invited
On 17 Mar, 2020
Version 1
Posted 15 Jan, 2020
No comments provided
Editorial decision: Major revision
On 10 Feb, 2020
Review #2 received
Received 09 Feb, 2020
Review #1 received
Received 04 Feb, 2020
Reviewer #2 agreed
On 25 Jan, 2020
Reviewer #1 agreed
On 21 Jan, 2020
Reviewers invited
Invitations sent on 17 Jan, 2020
Editor assigned
On 13 Jan, 2020
Submission checks complete
On 12 Jan, 2020
Editor invited
On 12 Jan, 2020
First submitted
On 09 Jan, 2020
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A new preprint design is coming!
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See the published version of this preprint at Journal of Biological Engineering.
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
Elizabeth Vargis
Utah State University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3141-9317
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 Journal of Biological Engineering.
No community comments so far
Editorial decision: Accept
On 23 Mar, 2020
Review #1 received
Received 20 Mar, 2020
Review #2 received
Received 20 Mar, 2020
Reviewers invited
Invitations sent on 19 Mar, 2020
Reviewer #1 agreed
On 19 Mar, 2020
Reviewer #2 agreed
On 19 Mar, 2020
Editor assigned
On 18 Mar, 2020
Submission checks complete
On 17 Mar, 2020
Editor invited
On 17 Mar, 2020
Version 1
Posted 15 Jan, 2020
No comments provided
Editorial decision: Major revision
On 10 Feb, 2020
Review #2 received
Received 09 Feb, 2020
Review #1 received
Received 04 Feb, 2020
Reviewer #2 agreed
On 25 Jan, 2020
Reviewer #1 agreed
On 21 Jan, 2020
Reviewers invited
Invitations sent on 17 Jan, 2020
Editor assigned
On 13 Jan, 2020
Submission checks complete
On 12 Jan, 2020
Editor invited
On 12 Jan, 2020
First submitted
On 09 Jan, 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 Journal of Biological Engineering.
Background Choroidal neovascularization (CNV) is a major cause of blindness in patients with age-related macular degeneration. CNV is characterized by new blood vessel growth and subretinal fluid accumulation, which results in mechanical pressure on retinal pigment epithelial (RPE) cells. Overexpressing RPE-derived angiogenic factors plays an important role in inducing CNV.
Results The goal of this study was to determine whether low levels of acute mechanical stress during early CNV can induce the expression of angiogenic factors in RPE cells and accelerate angiogenesis. Using a novel device, acute mechanical stress was applied to primary porcine RPE cells and the resulting changes in the expression of major angiogenic factors were examined using immunocytochemistry, qRT-PCR, and ELISA. An in vitro tube formation assay was used to determine the effect of mechanical stress on RPE cells on angiogenesis. Our results showed an increase in the expression of major angiogenic factors in response to mechanical stress, resulting in increased in vitro angiogenesis. Abnormal epithelial-mesenchymal transition (EMT) in RPE cells is also associated with CNV and further retinal degeneration. Our qRT-PCR results verified an increase in the expression of EMT genes in RPE cells.
Conclusions In conclusion, we showed that acute mechanical stress induces the expression of major angiogenic and EMT factors and promotes in vitro angiogenesis, suggesting that mechanical stress plays a role in promoting aberrant angiogenesis in AMD.
Figure 1
Figure 2
Figure 3
Figure 4
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