Article

Regulated expression of pancreatic triglyceride lipase after rat traumatic brain injury.

Cytoneurobiology Unit & Laboratory of Aging and Nervous Diseases, Medical College of Soochow University, Suzhou Industrial Park, Suzhou, Jiangsu 215123, People's Republic of China.
Molecular and Cellular Biochemistry (Impact Factor: 2.39). 09/2009; 335(1-2):127-36. DOI: 10.1007/s11010-009-0249-4
Source: PubMed

ABSTRACT Pancreatic triglyceride lipase (PTL), an enzyme of digestive system, plays very important roles in the digestion and absorption of lipids. However, its distribution and function in the central nervous system (CNS) remains unclear. In the present study, we mainly investigated the expression and cellular localization of PTL during traumatic brain injury (TBI). Western blot and RT-PCR analysis revealed that PTL was present in normal rat brain cortex. It gradually increased, reached a peak at the 3rd day after TBI, and then decreased. Double immunofluorescence staining showed that PTL was co-expressed with neuron, but had a few colocalizations in astrocytes. When TBI occurred in the rat cortex, the expression of PTL gradually increased, reached the peak at the 3rd day after TBI, and then decreased. Importantly, more PTL was colocalized with astrocytes, which is positive for proliferating cell nuclear antigen (PCNA). In addition, Western blot detection showed that the 3rd day post injury was not only the proliferation peak indicated by the elevated expression of PCNA, glial fibrillary acidic protein (GFAP) and cyclin D1, but also the apoptotic peak implied by the alteration of caspase-3 and bcl-2. These data suggested that PTL may be involved in the pathophysiology of TBI and PTL may be complicated after injury, more PTL was colocalized with astrocytes. Importantly, injury-induced expression of PTL was colabelled by proliferating cell nuclear antigen (proliferating cells marker), and the western blot for GFAP, PCNA and cyclin D1, showed that 3 days post injury was the proliferation peak, in coincidence to it, the protein level change of caspase-3 and bcl-2 revealed that the stage was peak of apoptotic too. These data suggested that PTL may be involved in the pathophysiology of TBI and that PTL may be implicated in the proliferation of astrocytes and the recovery of neurological outcomes. But the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of PTL after brain injury.

0 Followers
 · 
90 Views
  • Source
    • "However, while effective for research focused on isolated cellular mechanisms and pathways, in vitro models are incapable of capturing the in vivo complexity of the multi-cellular local, regional, and global brain networks and systemic responses in a whole animal to TBI. Commonly used TBI in vivo models include blast injury (Saljo et al., 2000), lesion administration (Bederson et al., 1986; Persson, 1976), microknife lesion ( Jia et al., 2010), weight drop impact (Valable et al., 2010), fluid percussion injury (FPI; Millen et al., 1985; Povlishock and Kontos, 1985), and the most common method, controlled cortical impact (CCI; Dixon et al., 1991; Lighthall, 1988). Briefly, both CCI and FPI involve exposing the animal skull with a midline incision along the scalp, followed by performing a craniotomy above the region of interest, usually centered 1–3 mm lateral to the midline while the animal is anesthetized. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Neurological dysfunction after traumatic brain injury (TBI) is caused by both the primary injury and a secondary cascade of biochemical and metabolic events. Since TBI can be caused by a variety of mechanisms, numerous models have been developed to facilitate its study. The most prevalent models are controlled cortical impact and fluid percussion injury. Both typically use "sham" (craniotomy alone) animals as controls. However, the sham operation is objectively damaging, and we hypothesized that the craniotomy itself may cause a unique brain injury distinct from the impact injury. To test this hypothesis, 38 adult female rats were assigned to one of three groups: control (anesthesia only); craniotomy performed by manual trephine; or craniotomy performed by electric dental drill. The rats were then subjected to behavioral testing, imaging analysis, and quantification of cortical concentrations of cytokines. Both craniotomy methods generate visible MRI lesions that persist for 14 days. The initial lesion generated by the drill technique is significantly larger than that generated by the trephine. Behavioral data mirrored lesion volume. For example, drill rats have significantly impaired sensory and motor responses compared to trephine or naïve rats. Finally, of the seven tested cytokines, KC-GRO and IFN-γ showed significant increases in both craniotomy models compared to naïve rats. We conclude that the traditional sham operation as a control confers profound proinflammatory, morphological, and behavioral damage, which confounds interpretation of conventional experimental brain injury models. Any experimental design incorporating "sham" procedures should distinguish among sham, experimentally injured, and healthy/naïve animals, to help reduce confounding factors.
    Journal of neurotrauma 12/2010; 28(3):359-69. DOI:10.1089/neu.2010.1427 · 3.97 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The protein TFIIB is a general transcription initiation factor that plays a pivotal role in the preinitiation complex (PIC) and selects the transcription initiation site. However, its distribution and function in the central nervous system (CNS) remains unclear. In the present study, we mainly investigated the expression and cellular localization of TFIIB during traumatic brain injury (TBI). Western blot analysis revealed that TFIIB was present in normal rat brain cortex. It gradually increased, reached a peak at the 5th day after TBI, and then decreased. Importantly, more TFIIB was colocalized with astrocytes and microglia, which are largely proliferated. In addition, Western blot detection showed that the 5th day post injury was also the proliferation peak indicated by the elevated expression of PCNA. Importantly, injury-induced expression of TFIIB was colabelled by proliferating cell nuclear antigen (proliferating cells marker). These data suggested that TFIIB may be implicated in the proliferation of astrocytes and microglia and the recovery of neurological outcomes. But the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of TFIIB after brain injury.
    Journal of molecular histology 06/2011; 42(3):265-71. DOI:10.1007/s10735-011-9330-x · 1.98 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: HBOC-201 may alter lipase and amylase detection on chemistry analyzers using optical methods and affect pancreatic function after trauma. Amylase and lipase measurements were correlated against HBOC-201 to evaluate interference on samples spiked with 0-6g/dL HBOC-201. The detection threshold was 2.5g/dL or none when measured, respectively, on Vitros 250 or Advia 1650 instruments. Amylase and lipase from blood samples collected from 55% EBV hemorrhaged Yucatan min-pigs showed peaks around 24-48 hours. Amylase increase was not significant between treatments but lipase was higher in HBOC-201-treated animals. Animals particularly affected by the injury had elevated enzymes after hemorrhagic shock, without significant clinical consequences.
    Artificial Cells Blood Substitutes and Biotechnology (formerly known as Artificial Cells Blood Substitutes and Immobilization Bi 06/2011; 39(3):155-61. DOI:10.3109/10731199.2010.516260 · 0.71 Impact Factor
Show more