Photobiomodulation is a widely used tool in regenerative medicine thanks to its ability to modulate a plethora of physiological responses. Wound re-epithelialization is strictly regulated by locally produced chemical mediators, such as nitric oxide (NO), a highly reactive free radical generated by the nitric oxide synthase (NOS) enzymatic family. In this study, it has been hypothesized that a 980-nm low-level laser stimulation could increase NO production in human keratinocytes and that such event might be directly related to the re-epithelialization process. Human keratinocytes were irradiated with increasing energy outputs (10–75 J) in the absence or presence of L-NAME, a NOS inhibitor. Laser stimulation induced an increase in NO production, resulting in an energy-dependent increase in both keratinocytes proliferation and re-epithelialization ability. The direct link between increased NO production and the observed physiological responses was confirmed by their inhibition in L-NAME pre-treated samples. Since NO production increase is a quick event, it is conceivable that it is due to an increase in existing NOS activity rather than to a de novo protein synthesis. For this reason, it could be hypothesized that photobiomodulation-derived NO positive effects on keratinocytes behavior might rely on a near infrared mediated increase in NOS conformational stability and cofactors as well as substrate binding ability, finally resulting in an increased enzymatic activity.

Photobiomodulation induces in vitro re-epithelialization via nitric oxide production / M. Rizzi, M. Migliario, S. Tonello, V. Rocchetti, F. Renò. - In: LASERS IN MEDICAL SCIENCE. - ISSN 0268-8921. - 33:5(2018 Jul), pp. 1003-1008. [10.1007/s10103-018-2443-7]

Photobiomodulation induces in vitro re-epithelialization via nitric oxide production

F. Renò
Ultimo
2018

Abstract

Photobiomodulation is a widely used tool in regenerative medicine thanks to its ability to modulate a plethora of physiological responses. Wound re-epithelialization is strictly regulated by locally produced chemical mediators, such as nitric oxide (NO), a highly reactive free radical generated by the nitric oxide synthase (NOS) enzymatic family. In this study, it has been hypothesized that a 980-nm low-level laser stimulation could increase NO production in human keratinocytes and that such event might be directly related to the re-epithelialization process. Human keratinocytes were irradiated with increasing energy outputs (10–75 J) in the absence or presence of L-NAME, a NOS inhibitor. Laser stimulation induced an increase in NO production, resulting in an energy-dependent increase in both keratinocytes proliferation and re-epithelialization ability. The direct link between increased NO production and the observed physiological responses was confirmed by their inhibition in L-NAME pre-treated samples. Since NO production increase is a quick event, it is conceivable that it is due to an increase in existing NOS activity rather than to a de novo protein synthesis. For this reason, it could be hypothesized that photobiomodulation-derived NO positive effects on keratinocytes behavior might rely on a near infrared mediated increase in NOS conformational stability and cofactors as well as substrate binding ability, finally resulting in an increased enzymatic activity.
keratinocytes; low-level laser therapy; nitric oxide; re-epithelialization; surgery
Settore BIO/16 - Anatomia Umana
lug-2018
Article (author)
File in questo prodotto:
File Dimensione Formato  
s10103-018-2443-7.pdf

accesso riservato

Tipologia: Publisher's version/PDF
Dimensione 570.58 kB
Formato Adobe PDF
570.58 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
2018+LASER+MED+SC++photobiomoduletions+LMS.pdf

accesso riservato

Tipologia: Publisher's version/PDF
Dimensione 570.61 kB
Formato Adobe PDF
570.61 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/1020238
Citazioni
  • ???jsp.display-item.citation.pmc??? 7
  • Scopus 26
  • ???jsp.display-item.citation.isi??? 25
social impact