Pepsin pretreatment allows collagen IV immunostaining of blood vessels in adult mouse brain

Franciosi, Sonia; Gasperi, Rita De; Dickstein, Dara L.; English, Daniel F.; Rocher, Anne B.; Janssen, William G.M.; Christoffel, Daniel J.; Sosa, Miguel A. Gama; Hof, Patrick R.; Buxbaum, Joseph D.; Elder, Gregory A.

doi:10.1016/j.jneumeth.2007.02.020

Cited by 49 publications

(52 citation statements)

References 36 publications

(42 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This observation is consistent with the results of earlier studies that have also described a considerable increase in signal intensity at sites of cerebral lesions [41]. It has been reported that this phenomenon is provoked by the breakdown of the neurovascular unit, which leaves the corresponding epitopes accessible for the antibodies, a development that is reversed upon the re-establishment of gliovascular junctions [42].…”

Section: Discussionsupporting

confidence: 93%

Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion

Kaiser

Penk

Franke

et al. 2016

Purinergic Signalling

View full text Add to dashboard Cite

Effective therapeutic measures against the development of brain edema, a life-threatening complication of cerebral ischemia, are necessary to improve the functional outcome for the patient. Here, we identified a beneficial role of purinergic receptor P2X7 activation in acute ischemic stroke. Involvement of P2X7 in the development of neurological deficits, infarct size, brain edema, and glial responses after ischemic cerebral infarction has been analyzed. Neurologic evaluation, magnetic resonance imaging, and immunofluorescence assays were used to characterize the receptor's effect on the disease progress during 72 h after transient middle cerebral artery occlusion (tMCAO). Sham-operated animals were included in all experiments for control purposes. We found P2X7-deficient mice to develop a more prominent brain edema with a trend towards more severe neurological deficits 24 h after tMCAO. Infarct sizes, T2 times, and apparent diffusion coefficients did not differ significantly between wild-type and P2X7 −/− animals.Our results show a characteristic spatial distribution of reactive glia cells with strongly attenuated microglia activation in P2X7 −/− mice 72 h after tMCAO. Our data indicate that P2X7 exerts a role in limiting the early edema formation, possibly by modulating glial responses, and supports later microglia activation.

show abstract

Section: Discussionsupporting

confidence: 93%

Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion

Kaiser

Penk

Franke

et al. 2016

Purinergic Signalling

View full text Add to dashboard Cite

show abstract

“…9 Immunostaining for collagen IV required pepsin pretreatment, as described previously. 17 Detailed information on all primary antibodies including dilutions for immunohistochemistry is provided in Table 1. Immunohistochemical detection was performed using the Vector ABC Elite kit (Vector Laboratories, Burlingame, CA), according to the supplier's instructions.…”

Section: Immunohistochemistry and Special Stainsmentioning

confidence: 99%

Brain-Specific Deletion of Extracellular Signal-Regulated Kinase 2 Mitogen-Activated Protein Kinase Leads to Aberrant Cortical Collagen Deposition

Heffron

Landreth

Samuels

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

The mitogen-activated protein kinases extracellular signal-regulated kinase (ERK)1 and 2 are essential intracellular mediators of numerous transmembrane signals. To investigate neural-specific functions of ERK2 in the brain, we used a Cre/lox strategy using Nestin:Cre to drive recombination in neural precursor cells. Nestin:Cre;ERK2 fl/fl conditional knockout (cKO) mice have architecturally normal brains and no gross behavioral deficits. However, all cKO mice developed early-onset (postnatal day 35 to 40) frontal cortical astrogliosis, without evidence of neuronal degeneration. Frontoparietal cortical gray matter, but not underlying white matter, was found to contain abundant pericapillary and parenchymal reticulin fibrils, which were shown by immunohistochemistry to contain fibrillar collagens, including type I collagen. ERK1 general KO mice showed neither fibrils nor astrogliosis, indicating a specific role for ERK2 in the regulation of brain collagen. Collagen fibrils were also observed to a lesser extent in GFAP:Cre;ERK2 The extracellular signal-regulated kinase (ERK) family of mitogen-activated protein kinases (MAPKs) has been intensely studied for roles in brain development, including control of both axonal 1,2 and dendritic 3 growth. Astroglial process extension is also dependent on ERK signaling. 4 Recent work strongly implicates ERK-mediated signaling in synaptic plasticity and memory formation, and mutations in ERK2 and other ERK pathway components are known to underlie some forms of inherited human cognitive disorders.5-7 ERK MAPK activation is also linked to astroglial activation in several forms of central nervous system (CNS) injury. 8 -10 To directly test the importance of ERK MAPKs in vivo, gene knockout approaches are needed. Whereas ERK1 general knockout (KO) mice are viable and have architecturally normal brains, 11 general KO of ERK2 is embryonic lethal, because of defects in mesoderm differentiation and placental development.12-14 Thus, conditional KO (cKO) strategies are necessary to study brain-specific roles of ERK2. Two recent reports 15,16 describe aspects of the developmental phenotype resulting from CNS-specific KO of the mapk1 gene, encoding ERK2. We now present a novel aspect of the adult phenotype of a brain-specific ERK2 cKO driven by Nestin:Cre. Our findings suggest an unexpected and specific role for this classical MAPK member in the regulation of brain collagen deposition. Materials and Methods Transgenic Mice and PCR GenotypingThe generation of strain harboring a conditional ("floxed") mapk1 mutant allele (Mapk1 flox/flox ; subsequently referredSupported by grants NS047378 (to J.W.M.) and NS032779, MH57014, NS13546, and NS057098 (to G.E.L.).

show abstract

“…The green fluorescent protein (GFP) was detected using a rabbit polyclonal antibody raised against GFP that was isolated directly from A. victoria and purified by ion-exchange to remove nonspecific Ig (Invitrogen) (Franciosi et al, 2007). Immunoperoxidase experiments: The GFP immunodetection was performed as previously described (Ahmed et al, 2010).…”

Section: Rodent Experimentsmentioning

confidence: 99%

l-DOPA Impairs Proteasome Activity in Parkinsonism through D₁Dopamine Receptor

Berthet¹,

Bézard²,

Porras³

et al. 2012

J. Neurosci.

View full text Add to dashboard Cite

Aberrant membrane localization of dopamine D 1 receptor (D1R) is associated with L-DOPA-induced dyskinesia (LID), a major complication of L-DOPA treatment in Parkinson's disease (PD). Since the proteasome plays a central role in modulating neuronal response through regulation of neurotransmitter receptor intraneuronal fate, we hypothesized that the ubiquitine-proteasome proteolytic pathway could be impaired in LID. Those LIDs are actually associated with a striatum-specific decrease in proteasome catalytic activity and accumulation of polyubiquitinated proteins in experimental rodent and monkey parkinsonism. We then demonstrated that such decreased proteasome catalytic activity (1) results from D1R activation and (2) feed-back the D1R abnormal trafficking, i.e., its exaggerated cell surface abundance. We further showed that the genetic invalidation of the E3 ubiquitin-protein ligase parkin PD gene leads to exaggerated abnormal involuntary movements compared with wild-type mice. We thus established in an unprecedented series of experimental models that impairment of the ubiquitine-proteasome system at specific nodes (E3 ligase parkin, polyubiquitination, proteasome catalytic activity) leads to the same phenomenon, i.e., aberrant behavioral response to dopamine replacement therapy in PD, highlighting the intimate interplay between dopamine receptor and proteasome activity in a nondegenerative context.

show abstract

Pepsin pretreatment allows collagen IV immunostaining of blood vessels in adult mouse brain

Cited by 49 publications

References 36 publications

Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion

Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion

Brain-Specific Deletion of Extracellular Signal-Regulated Kinase 2 Mitogen-Activated Protein Kinase Leads to Aberrant Cortical Collagen Deposition

l-DOPA Impairs Proteasome Activity in Parkinsonism through D₁Dopamine Receptor

Contact Info

Product

Resources

About

Pepsin pretreatment allows collagen IV immunostaining of blood vessels in adult mouse brain

Cited by 49 publications

References 36 publications

Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion

Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion

Brain-Specific Deletion of Extracellular Signal-Regulated Kinase 2 Mitogen-Activated Protein Kinase Leads to Aberrant Cortical Collagen Deposition

l-DOPA Impairs Proteasome Activity in Parkinsonism through D1Dopamine Receptor

Contact Info

Product

Resources

About

l-DOPA Impairs Proteasome Activity in Parkinsonism through D₁Dopamine Receptor