Cyclic AMP

Lasers Med Sci.  2011 May;26(3):389-400. Epub 2010 Dec 24.

Low-level laser therapy (LLLT) acts as cAMP-elevating agent in acute respiratory distress syndrome.

de Lima FM, Moreira LM, Villaverde AB, Albertini R, Castro-Faria-Neto HC, Aimbire F.

Source

Research and Development Institute – IP&D, Av. Shishima Hifumi, 2911 – Urbanova, Po Box 12244-00, São José dos Campos, SP, Brazil.

Abstract

The aim of this work was to investigate if the low-level laser therapy (LLLT) on acute lung inflammation (ALI) induced by lipopolysaccharide (LPS) is linked to tumor necrosis factor (TNF) in alveolar macrophages (AM) from bronchoalveolar lavage fluid (BALF) of mice. LLLT has been reported to actuate positively for relieving the late and early symptoms of airway and lung inflammation. It is not known if the increased TNF mRNA expression and dysfunction of cAMP generation observed in ALI can be influenced by LLLT. For in vivo studies, Balb/c mice (n?=?5 for group) received LPS inhalation or TNF intra nasal instillation and 3 h after LPS or TNF-?, leukocytes in BALF were analyzed. LLLT administered perpendicularly to a point in the middle of the dissected bronchi with a wavelength of 660 nm and a dose of 4.5 J/cm(2). The mice were irradiated 15 min after ALI induction. In vitro AM from mice were cultured for analyses of TNF mRNA expression and protein and adenosine3′:5′-cyclic monophosphate (cAMP) levels. One hour after LPS, the TNF and cAMP levels in AM were measured by ELISA. RT-PCR was used to measure TNF mRNA in AM. The LLLT was inefficient in potentiating the rolipram effect in presence of a TNF synthesis inhibitor. LLLT attenuated the neutrophil influx and TNF in BALF. In AM, the laser increased the cAMP and reduced the TNF-? mRNA. LLLT increases indirectly the cAMP in AM by a TNF-dependent mechanism.

Br J of Dermatol.  2009 Aug;161(2):273-80. Epub 2009 Apr 30.

Low-energy helium-neon laser induces melanocyte proliferation via interaction with type IV collagen: visible light as a therapeutic option for vitiligo.

Lan CC, Wu CS, Chiou MH, Chiang TY, Yu HS.

Source

Department of Dermatology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.

Abstract

BACKGROUND:

The treatment of vitiligo remains a challenge for clinical dermatologists. We have previously shown that the helium-neon laser (He-Ne laser, 632.8 nm) is a therapeutic option for treatment of this depigmentary disorder.

OBJECTIVES:

Addressing the intricate interactions between melanocytes, the most important cellular component in the repigmentation scheme of vitiligo, and their innate extracellular matrix collagen type IV, the current study aimed to elucidate the effects of the He-Ne laser on melanocytes.

METHODS:

Cultured melanocytes were irradiated with the He-Ne laser. Relevant biological parameters including cell attachment, locomotion and growth were evaluated. In addition, the potentially involved molecular pathways were also determined.

RESULTS:

Our results show that in addition to suppressing mobility but increasing attachment to type IV collagen, the He-Ne laser stimulates melanocyte proliferation through enhanced alpha2beta1 integrin expression. The expression of phosphorylated cyclic-AMP response element binding protein (CREB), an important regulator of melanocyte growth, was also upregulated by He-Ne laser treatment. Using a specific mitochondrial uncoupling agent [carbonyl cyanide m-chlorophenyl-hydrazone (CCCP)], the proliferative effect of the He-Ne laser on melanocytes was abolished and suppression of melanocyte growth was noted.

CONCLUSIONS:

In summary, we have demonstrated that the He-Ne laser imparts a growth stimulatory effect on functional melanocytes via mitochondria-related pathways and proposed that other minor pathways including DNA damage may also be inflicted by laser treatment on irradiated cells. More importantly, we have completed the repigmentation scheme of vitiligo brought about by He-Ne laser light in vitro and provided a solid theoretical basis regarding how the He-Ne laser induces recovery of vitiligo in vivo.

Photochem Photobiol.  2009 Jul-Aug;85(4):987-96. Epub 2009 Feb 13.

Mitochondrial responses of normal and injured human skin fibroblasts following low level laser irradiation–an in vitro study.

Zungu IL, Hawkins Evans D, Abrahamse H.

Source

Laser Research Group, Faculty of Health Sciences, University of Johannesburg, Johannesburg, South Africa.

Abstract

Laser irradiation has proved to be very efficient in speeding and improving the quality of healing in pathological conditions of diverse etiologies. However, the mechanisms by which the beneficial effects are attained are not clear. Mitochondria are the primary phototargets during irradiation. The study aimed to establish if laser irradiation had an effect on hypoxic and acidotic cells. The study also aimed to use existing information regarding the possible mechanism of action (established in wounded cells) and apply these principles to acidic and hypoxic irradiated cells to determine whether laser has a stimulatory or inhibitory effect. Cell cultures were modified to simulate conditions of hypoxia (hypoxic gas mixture 95% N2 and 5% O2) and acidosis (pH 6.7) whereas the central scratch model was used to simulate a wound. Cells were irradiated with a helium-neon (632.8 nm, 3 mW cm(-2)) laser using 5 or 16 J cm(-2) on days 1 and 4. Mitochondrial responses were measured 1 or 24 h after laser irradiation by assessing changes in mitochondrial membrane potential (MMP), cyclic AMP, intracellular Ca2+ and adenosine triphosphate (ATP) cell viability. Hypoxia and acidosis significantly reduced MMP when compared with normal nonirradiated control cells. Wounded, hypoxic and acidotic cells irradiated with 5 J cm(-2) showed an increase in mitochondrial responses when compared with nonirradiated cells while 16 J cm(-2) showed a significant decrease. The study confirmed that laser irradiation with 5 J cm(-2) stimulated an increase in intracellular Ca2+ which resulted in an increase in MMP, ATP and cAMP, which ultimately results in photobiomodulation to restore homeostasis of injured cells.