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PPL‐240 modulates VEGF‐A secretion by HMC‐1 after ultraviolet radiation (UVR)

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Mast cells may be recruited by tumor‐derived chemoattractants and selectively secrete molecules such as VEGF that permit the formation of new blood vessels and metastases. We analyze the VEGF‐A and C secretion by HMC‐1 after UVR and their modulation by Polypodium leucotomos extract (PPL‐240). HMC‐1 cells were incubated for 2h in presence or absence of PPL‐240 and exposed to UVR (HB406). Finally, cells were culture in presence or absence of PMA during 24h in order to induce the secretion of soluble mediators. VEGF‐A and ‐C levels were determined by ELISA. UVR increased VEGF‐A levels by 65% (70±13 to 116±24 pg/ml) (p<0.018), levels that stay at baseline in PPL‐240‐treated cells. When UVR exposed cells were treated with PMA, VEGF‐A levels were amplified (over 278%, 324±136 pg/ml) (p<0.001) in comparison to irradiated and PMA untreated cells (p<0.001) and to irradiated and treated with PMA (74±6 pg/ml) (p<0.002). PPL‐240 reduced its release reaching to control levels in PMA untreated HMC‐1 (65±3 pg/ml) and in PMA treated HMC‐1 (79±11 pg/ml) (p<0.012) after UVR exposure. Regarding VEGF‐C secretion, UVR did not altered its levels with and without PPL‐240 treatment. PMA addition reduced the levels of VEGF‐C induced by UV‐exposed cells (118±17 to 95±10 pg/ml). We conclude that UVR increases VEGF‐A by HMC‐1 and PPL‐240 treatment normalizes these levels, which may be relevant for reducing tumour growth and metastasis.
Title: PPL‐240 modulates VEGF‐A secretion by HMC‐1 after ultraviolet radiation (UVR)
Description:
Mast cells may be recruited by tumor‐derived chemoattractants and selectively secrete molecules such as VEGF that permit the formation of new blood vessels and metastases.
We analyze the VEGF‐A and C secretion by HMC‐1 after UVR and their modulation by Polypodium leucotomos extract (PPL‐240).
HMC‐1 cells were incubated for 2h in presence or absence of PPL‐240 and exposed to UVR (HB406).
Finally, cells were culture in presence or absence of PMA during 24h in order to induce the secretion of soluble mediators.
VEGF‐A and ‐C levels were determined by ELISA.
UVR increased VEGF‐A levels by 65% (70±13 to 116±24 pg/ml) (p<0.
018), levels that stay at baseline in PPL‐240‐treated cells.
When UVR exposed cells were treated with PMA, VEGF‐A levels were amplified (over 278%, 324±136 pg/ml) (p<0.
001) in comparison to irradiated and PMA untreated cells (p<0.
001) and to irradiated and treated with PMA (74±6 pg/ml) (p<0.
002).
PPL‐240 reduced its release reaching to control levels in PMA untreated HMC‐1 (65±3 pg/ml) and in PMA treated HMC‐1 (79±11 pg/ml) (p<0.
012) after UVR exposure.
Regarding VEGF‐C secretion, UVR did not altered its levels with and without PPL‐240 treatment.
PMA addition reduced the levels of VEGF‐C induced by UV‐exposed cells (118±17 to 95±10 pg/ml).
We conclude that UVR increases VEGF‐A by HMC‐1 and PPL‐240 treatment normalizes these levels, which may be relevant for reducing tumour growth and metastasis.

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